Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 2649 2022-11-11 00:42:06 |
2 update references and layout + 5 word(s) 2654 2022-11-11 03:17:42 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Shree, N.;  Ding, Z.;  Flaws, J.;  Choudhury, M. microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health. Encyclopedia. Available online: https://encyclopedia.pub/entry/33967 (accessed on 15 June 2024).
Shree N,  Ding Z,  Flaws J,  Choudhury M. microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health. Encyclopedia. Available at: https://encyclopedia.pub/entry/33967. Accessed June 15, 2024.
Shree, Nitya, Zehuan Ding, Jodi Flaws, Mahua Choudhury. "microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health" Encyclopedia, https://encyclopedia.pub/entry/33967 (accessed June 15, 2024).
Shree, N.,  Ding, Z.,  Flaws, J., & Choudhury, M. (2022, November 11). microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health. In Encyclopedia. https://encyclopedia.pub/entry/33967
Shree, Nitya, et al. "microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health." Encyclopedia. Web. 11 November, 2022.
microRNA in Endocrine Disruptor-Induced Immunomodulation of Metabolic Health
Edit

Deteriorated metabolic health is rapidly becoming a serious public health burden across all genders, ages, and socioeconomic groups. Obesity is one of the leading causes of death, which impacts 35% of the US population and is predicted to increase to 42% by 2030. Additionally, medical expenditures for obesity-related conditions are expected to exceed 1 trillion USD by 2025. It is evident that the effort to treat and prevent obesity still requires improvement. Obesity has been primarily attributed to overnutrition, sedentary lifestyle, and genetic inheritance; however, it is unlikely that these are the only factors responsible for this exponential rise of the epidemic in recent years. Emerging evidence suggests that chronic exposure to environmental chemicals may contribute to the rapid rise in the prevalence of metabolic disorders. Additionally, disturbances during crucial developmental windows can promote subtle changes in gene expression, leading to modifications in biological and molecular processes. Ultimately, these modifications alter the developmental trajectory, leaving permanent, long-lasting metabolic dysfunction that may persist from adolescence to subsequent generations.

EDCs DOHaD innate immune system miRs

1.  Endocrine-Disrupting Chemicals (EDCs) Exposure and the Immune System

The progression of disease due to EDC exposure during development has been associated with alterations in the immune system of humans [1]. The immune system is a collaborative network of cells and proteins that protect the body against anything that is identified as non-self or foreign. It comprises bone marrow, the thymus, the spleen, white blood cells, antibodies, the complement system, and the lymphatic system [2]. The complementary machineries within the immune system are innate immunity and adaptive immunity. The innate immune response is the first line of defense that is activated to destroy intruding material. It is non-specific and acts via physical barriers (e.g., skin and mucous membrane, cilia) and chemical barriers (e.g., lysozyme, gastric juice, and saliva). The second line of defense is the adaptive immune response. It is designed to react against specific recognized antigens located on foreign material. It is carried out by the lymphocytes that are responsible for the development of immunological memory. Innate control of adaptive immunity plays a crucial role during the development of immune response, which further contributes to the activation of long-lasting adaptive immunity [3]. Exposure to EDCs can directly affect the innate immune response, contributing to endocrine imbalance [4]. Therefore, the focus is on the impact of EDCs on the innate immune system.
The innate immune system consists of monocytes, macrophages, mast cells, neutrophils, and natural killer cells [2]. Monocytes express various receptors capable of monitoring and sensing environmental changes. Typically, a monocyte cell circulates in the blood for about 1–3 days before migrating into the tissues where they differentiate into a macrophage or a dendritic cell. Monocytes and macrophages are one of the major sources of tumor necrosis factor-alpha (TNF-α) [5]. In a mouse macrophage cell line, EDCs can alter the inflammatory response and the host’s defense mechanism against pathogens [6]. Overall, this demonstrates that alteration in the TNF-α secretion pattern by macrophages at local disease sites is accompanied by the development of inflammatory diseases [7]. A study by Kuan et al. showed elevated levels of TNF-α secretion in RAW 264.7 cells exposed to bisphenol A (BPA), an industrial plasticizer [8]. One of the most recent meta-analyses conducted to investigate the link between EDCs and inflammatory markers in humans revealed that BPA exposure is linked to the differential levels of C-reactive protein (CRP) and IL-6 [9]. Di-2-ethylhexyl phthalate (DEHP) enhances TNF-α production from monocytes/macrophages in vitro and in vivo [7]. Studies have shown that EDCs, including DEHP, BPA, and dichlorodiphenyltrichloroethane (DDT), can modulate the production of several interleukins, such as IL-6, IL-8, IL-4, and IL-1β [10]. This implicates EDCs’ role in metabolic dysregulation because alteration in the inflammatory and non-inflammatory cytokine pools is a common scenario in metabolic disorders [11].
In addition to macrophages and monocytes, mast cells mediate inflammatory responses, such as allergic reactions and hypersensitivity. These cells are present throughout the connective tissue of the body. A limited amount of data reveal that degranulation of mast cells and eosinophilic infiltration can be induced by exposure to phthalates [12]. Triclosan, found in cosmetics and personal care products, has been shown to inhibit RBL-2H3 mast cells by decreasing the mitochondrial membrane potential that leads to the inhibition of mitochondrial translocation and ultimately reduces the influx of calcium ions into the cells [13]. Researchers have shown that mast cells can be activated by BPA, resulting in accelerated release of histamines and leukotrienes [14].

2. EDCs, MiR, and Innate Immunity

2.1. Impact of EDC Exposure on MiR Regulation

EDCs, including both natural and synthetic chemicals, are initially found to induce adverse health consequences through interruption of hormone receptors. This includes estrogen receptors and retinoid receptors [15], especially during development, reproductive, and metabolic regulations [16][17]. Some of the EDCs can bind to the receptor proteins directly and can regulate downstream target gene expression [18][19]. Recently, studies have suggested other mechanisms on how EDCs induce the progression of the diseases. MiRs, which are susceptible to cellular stresses and environmental exposures [20], have been found to be influenced by EDCs as well. One of the insightful underlying mechanisms is that EDCs can regulate the miRs through their targeted hormones or receptors. Different studies in cell lines, rodents, and other vertebrates suggest that the expression of miRs can be regulated by hormones [21][22][23][24]. A study using MCF-7 breast cancer cell lines has shown that miR transcriptome alteration was induced by BPA and DDT treatment [25]. In another study, researchers showed that the treatment with perfluorooctanesulfonate alters the expression levels of about 38 miRs that are involved in thyroid hormone dysregulation [22]. A few studies also proposed that EDCs can directly modulate the expression level of miRs in different tissues or cell lines connected to metabolism [26][27][28][29][30]. For example, the recent study showed that the miR-34a-5p level is upregulated by benzyl butyl phthalate (BBP), thus promoting adipogenesis in 3T3-L1 cells through Nampt and sirtuins regulation [27]. Additionally, the data indicated that mono-(2-ethylhexyl) phthalate can induce regulation of several miRs, which are responsive to oxidative stress in vitro [26]. Besides the regulation of metabolism, EDCs also affect the cellular inflammatory response through miR modulation [28][29][31]. An in vitro study demonstrated that BPA treatment can induce the expression of miR-146a-5p, which mediates inflammatory response [29]. Lastly, tetrachlorodibenzo-p-dioxin, a pharmaceutical ligand, was found to induce cholinergic anti-inflammation through the upregulation of miR-132 [32]. One clinical study suggested that polychlorinated biphenyls (PCBs), which have similar structures as dioxin, induce miR-191 expression in peripheral blood mononuclear cells. Pathway analysis also identifies several potential targets of miR-191 that are associated with immunomodulation [33]. Taken together, EDCs may play a substantial role in alteration of miR levels and in the regulation of immune response that possibly contributes to chronic diseases such as obesity.
To understand the health consequences induced by EDCs, research focus has widened from their effect on one generation to their impact on the next generation as well as multiple generations. Since EDCs are persistent in the environment, their impression is more likely to pass through several generations and can even skip one generation and carry through to the next [34][35][36]. Moreover, when considering the prenatal and postnatal effects of EDC exposure, the situation becomes more complicated and is still under development. The transgenerational effects of EDCs on miR expression levels have been reported in several rodent and other mammal models [37][38][39][40]. For example, a mouse study showed genistein and/or BPA exposure at the developmental stage significantly affects the offspring’s miR expression patterns in the brain, leading to behavioral and metabolic alteration [37]. Paternal benzo[a]pyrene exposure led to miR expression pattern alteration in the offspring mice, and pathway analysis showed enriched target genes related to cell metabolism [38].
Several underlying mechanisms have demonstrated how miRs may navigate their effect in the next generation. First, the epigenetic imprint of miR levels can be inherited through the sperm cells [41], as they are sensitive to environmental factors such as EDCs [40][42]. Although there is no direct evidence to show that the miR profiles in oocytes is affected by the maternal environment, the effects of EDCs on DNA methylation and histone modification have been well studied in oocytes [43][44]. A mouse study showed that the oocyte transcriptome is affected in type I diabetic females [45], and alteration of miR levels is very likely to be one of the underlying mechanisms.
Secondly, EDCs can act through modification of placental development to affect fetal intrauterine growth, although the mechanism is not fully understood [46]. One of the hormones that are significantly affected by EDCs, thyroid hormone, plays an important role in placental development [47][48]. Mounting evidence also shows that miRs regulate thyroid hormone signaling by targeting hormone synthesis and the expression level of its receptors [49]. On the other hand, miR expression can also be tuned by thyroid hormone [50][51]. In the mouse model, gestational DEHP exposure leads to thyroid hormone signaling disturbance and placenta malformation; this is accomplished through suppressing Thrα1 and Thrβ1 expression and their activity, ultimately causing fetal intrauterine growth restriction [52]. A cohort study also found that PCBs are associated with induced thyroid-stimulating hormone and thyroid hormone dysregulation in pregnant women [53]. This occurrence may lead to an adverse effect in the next generation, possibly through miR modulation. Other than that, in studies using in vivo or in vitro models, EDCs have been shown to affect other hormones such as human chorionic gonadotropin and corticotropin-releasing hormone along with impacting placental development through mechanisms including miR modulation [26][54][55][56][57]. It has been shown that exposure to BPA leads to miR-146a upregulation in both 3A and HTR-8 cells, potentially implicating its important role in inflammatory response and cell growth [54]. A study in the placental transcriptome also demonstrated that the miR-146a level is significantly upregulated and associated with BPA accumulation [58].
Lastly, Some EDCs can cross the placental barrier and reach the fetus, which would have a notable impact on its development [59][60][61]. EDCs can also be found in breast milk, while others are more likely to accumulate within the adipose tissue due to their hydrophobic nature [62]. These eventually provide prolonged adverse effects to those tissues. Due to this indirect exposure, fetal miR expression levels can be affected in different organs [37][39]. On the other hand, recent studies indicated that maternal miRs can traffic into the fetal side through the placental barrier [63]; this provides a new perspective of how the fetus can be affected by the external environment. These studies together implicate miR regulation in the transgenerational and postnatal effects of EDCs.

2.2. MiR in Innate Immunity

MiRs are expressed in various cells of the innate immune system such as monocytes, macrophages, dendritic cells, granulocytes, and NK cells [64]. They can rapidly respond to external stimuli [65]. Accumulating evidence indicates that miRs modulate immune responses at various steps of the innate immune network, including (1) production and release of cytokines/chemokines; (2) pattern recognition regulation; as well as (3) monocyte development and macrophage polarization.
Inflammatory cytokines are a large family of secretory proteins, which play a key role in immune response regulation and metabolic homeostasis maintenance. Studies have suggested that miRs play an essential role in transcriptional regulation and secretion of cytokines [66][67][68][69][70]. For example, miR-155 was found to promote TNF-α expression by directly binding to the transcripts of its inhibitors in RAW cells [68]. TNF-α can also induce the expression of miR-155 [69], suggesting a reciprocal regulation between miRs and cytokines levels. Furthermore, miR-145 was found to promote TNF-α expression and secretion in human adipocytes [67]; it can also increase the bioactivity of TNF-α through inhibiting metalloprotease 17 [71]. Studies have also shown that miRs are involved in the determination of macrophage inflammatory response, which plays a critical role in obesity [72][73][74][75]. In a study using human monocytes, miR-146b was induced by LPS or IL-10, which led to the further downregulation of a cluster of Toll-like receptor (TLR) signaling genes, suggesting an anti-inflammatory role of miR-146b [74]. In another study, miR-497 treatment was found to inhibit the expression of pro-inflammatory cytokines, such as TNF-α and IL-1β, under in vivo or in vitro settings [75]. These studies suggest that miR regulation on cytokine secretion can further affect immune responses and metabolic health.
Monocytes and macrophages are predominantly derived from hematopoietic stem cells (HSCs) [76], playing an important role in inflammation regulation and homeostasis maintenance in different tissues [77][78][79]. Recently, miRs were found to be involved in the differentiation of bone marrow HSCs and the maturation of circulating monocytes [80][81]. A considerable array of miRs is highly expressed in the HSCs, such as miR-125, miR-126, and miR-146 [82][83][84][85]. Interestingly, overexpression of miR-125a has been shown to enlarge the hematopoietic stem cell pool by targeting pro-apoptotic protein BAK1 [86]. This has been shown to play a role in obesity and other metabolic diseases [87][88]. On the contrary, miR-126 serves as an inhibitor for stem cell proliferation [83]. Furthermore, the HSCs commitment to macrophage progenitors is also related to miR levels, especially controlled by the PU.1, a transcriptional factor. MiR-17p-92 is suppressed by PU.1 during myeloid differentiation, leading to the downregulation of a subset of miRs involved in myeloid progenitor maintenance [89]. These studies suggest a potential role of miRs in controlling major stages of monocyte development from HSCs. Importantly, the stemness and niche size of HSCs are sensitive to metabolic homeostasis and found to be disrupted in obesity along with other metabolic diseases [87][88][90][91]. Therefore, the maintenance of tissue homeostasis is likely to be connected to miR profile integrity and may be a factor in the metabolic scenario.
As it was discussed at the beginning of the review, in metabolic tissues, such as the liver and adipose tissue, macrophages are key players in maintaining metabolic homeostasis [92]. Traditionally, macrophages are responsive to environmental cues that induce different pathways of cell differentiation to either M1 or M2. The phenotype associated with polarization towards M1 macrophages and secretion of pro-inflammatory cytokines is well characterized in many chronic diseases, such as obesity and nonalcoholic fatty liver disease [92]. Several reports suggested that miRs regulate either M1 or M2 polarization. For example, knockdown of miR-21 resulted in the reduction in M2 phenotype genes: arginase 1, mannose receptor 1, and IL-4Ra in vitro [93]. Furthermore, adipose tissue can produce or secrete a variety of pro-inflammatory and anti-inflammatory factors. This includes the adipokines leptin, adiponectin; resistin; as well as other cytokines and chemokines, such as TNF-α, IL-6, and MCP-1. These cytokines can stimulate macrophage polarization and produce negative feedback to the adipose tissue, therefore creating a vicious cycle [94][95]. Interestingly, in ewes, maternal obesity causes miR downregulation in the offspring’s muscle and further contributes to the upregulation of inflammatory cytokines [96]. Therefore, miRs can be an inevitable factor in the immune regulation and metabolic dysfunction. Overall, the interaction between miR profiles and inflammatory response has been extensively recognized and their roles in metabolic disease are significant.
In memoriam of Dr. Panzica, it would like to be stressed that EDCs also impact the neurological system as shown by his lifelong research. On this note, the understanding of miR functions is not limited to the metabolic processes mentioned above; it may also be expanded to include the modulation by miRs in other physiological activities [97][98][99][100]. A great number of studies indicate the tight connection between miRs and neural functions. A study showed that miR-219 was downregulated in a demyelinated mouse model via regulating MCT1 expression [101]. Another study on advanced paternal age (a risk factor for neurodevelopmental disorders) showed that miR-132 and miR-134 were both differentially regulated in rats and humans [102]. EDCs can affect the synthesis of various neuropeptides, hormones and enzymes, which results in an impact on the neural system and brain functions [103][104][105][106]. For example, Panzica group demonstrated that genistein affected the NO-producing cell number and induced significant changes in aggressive and anxiety behaviors in male mice [103]. In addition, whole-body metabolism and reproduction are also influenced by EDCs. Panzica group showed that postnatal genistein exposure induced body weight increase and significantly downregulated leptin and triiodothyronine, while the phenotypes were limited to female mice [104]. These studies suggested a potential mechanism of metabolism regulation by EDCs. Moreover, a study showed that expressions of several miRs in peripheral blood mononuclear cells were changed in anxiety disorder patients [107], suggesting a novel perspective link between miRs, immunity, and cognitive function.

References

  1. Howard, S.G. Developmental Exposure to Endocrine Disrupting Chemicals and Type 1 Diabetes Mellitus. Front. Endocrinol. 2018, 9, 513.
  2. Nowak, K.; Jabłońska, E.; Ratajczak-Wrona, W. Immunomodulatory Effects of Synthetic Endocrine Disrupting Chemicals on the Development and Functions of Human Immune Cells. Environ. Int. 2019, 125, 350–364.
  3. Iwasaki, A.; Medzhitov, R. Control of Adaptive Immunity by the Innate Immune System. Nat. Immunol. 2015, 16, 343–353.
  4. Bennasroune, A.; Rojas, L.; Foucaud, L.; Goulaouic, S.; Laval-Gilly, P.; Fickova, M.; Couleau, N.; Durandet, C.; Henry, S.; Falla, J. Effects of 4-Nonylphenol and/or Diisononylphthalate on Thp-1 Cells: Impact of Endocrine Disruptors on Human Immune System Parameters. Int. J. Immunopathol. Pharm. 2012, 25, 365–376.
  5. Lee, J.W.; Han, H.K.; Park, S.; Moon, E.Y. Nonylphenol Increases Tumor Formation and Growth by Suppressing Gender-Independent Lymphocyte Proliferation and Macrophage Activation. Environ. Toxicol. 2017, 32, 1679–1687.
  6. Couleau, N.; Falla, J.; Beillerot, A.; Battaglia, E.; Innocenzo, M.D.; Plancon, S.; Laval-Gilly, P.; Bennasroune, A. Effects of Endocrine Disruptor Compounds, Alone or in Combination, on Human Macrophage-Like Thp-1 Cell Response. PLoS ONE 2015, 10, e0131428.
  7. Hansen, J.F.; Bendtzen, K.; Boas, M.; Frederiksen, H.; Nielsen, C.H.; Rasmussen, K.; Feldt-Rasmussen, U. Influence of Phthalates on Cytokine Production in Monocytes and Macrophages: A Systematic Review of Experimental Trials. PLoS ONE 2015, 10, e0120083.
  8. Kuan, Y.H.; Li, Y.C.; Huang, F.M.; Chang, Y.C. The Upregulation of Tumour Necrosis Factor-A and Surface Antigens Expression on Macrophages by Bisphenol a-Glycidyl-Methacrylate. Int. Endod. J. 2012, 45, 619–626.
  9. Liu, Z.; Lu, Y.; Zhong, K.; Wang, C.; Xu, X. The Associations between Endocrine Disrupting Chemicals and Markers of Inflammation and Immune Responses: A Systematic Review and Meta-Analysis. Ecotoxicol. Environ. Saf. 2022, 234, 113382.
  10. Ochiai, S.; Roediger, B.; Abtin, A.; Shklovskaya, E.; De St Groth, B.F.; Yamane, H.; Weninger, W.; Le Gros, G.; Ronchese, F. Cd326(Lo)Cd103(Lo)Cd11b(Lo) Dermal Dendritic Cells Are Activated by Thymic Stromal Lymphopoietin During Contact Sensitization in Mice. J. Immunol. 2014, 193, 2504–2511.
  11. Makki, K.; Froguel, P.; Wolowczuk, I. Adipose Tissue in Obesity-Related Inflammation and Insulin Resistance: Cells, Cytokines, and Chemokines. ISRN Inflamm. 2013, 2013, 139239.
  12. Bornehag, C.G.; Nanberg, E. Phthalate Exposure and Asthma in Children. Int. J. Androl. 2010, 33, 333–345.
  13. Weatherly, L.M.; Nelson, A.J.; Shim, J.; Riitano, A.M.; Gerson, E.D.; Hart, A.J.; de Juan-Sanz, J.; Ryan, T.A.; Sher, R.; Hess, S.T.; et al. Antimicrobial Agent Triclosan Disrupts Mitochondrial Structure, Revealed by Super-Resolution Microscopy, and Inhibits Mast Cell Signaling Via Calcium Modulation. Toxicol. Appl. Pharmacol. 2018, 349, 39–54.
  14. O’brien, E.; Dolinoy, D.C.; Mancuso, P. Bisphenol a at Concentrations Relevant to Human Exposure Enhances Histamine and Cysteinyl Leukotriene Release from Bone Marrow-Derived Mast Cells. J. Immunotoxicol. 2014, 11, 84–89.
  15. Diamanti-Kandarakis, E.; Bourguignon, J.-P.; Giudice, L.C.; Hauser, R.; Prins, G.S.; Soto, A.M.; Zoeller, R.T.; Gore, A.C. Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement. Endocr. Rev. 2009, 30, 293–342.
  16. Gouesse, R.J.; Plante, I. Environmental Exposure to Bfrs: Unraveling Endocrine and Mammary Gland Effects That May Increase Disease Risk. Toxicol. Sci. 2022, 186, 190–207.
  17. Ehrlich, S.; Lambers, D.; Baccarelli, A.; Khoury, J.; Macaluso, M.; Ho, S.M. Endocrine Disruptors: A Potential Risk Factor for Gestational Diabetes Mellitus. Am. J. Perinatol. 2016, 33, 1313–1318.
  18. Wolstenholme, J.T.; Rissman, E.F.; Connelly, J.J. The Role of Bisphenol a in Shaping the Brain, Epigenome and Behavior. Horm. Behav. 2011, 59, 296–305.
  19. Hafezi, S.A.; Abdel-Rahman, W.M. The Endocrine Disruptor Bisphenol a (Bpa) Exerts a Wide Range of Effects in Carcinogenesis and Response to Therapy. Curr. Mol. Pharmacol. 2019, 12, 230–238.
  20. Miguel, V.; Cui, J.Y.; Daimiel-Ruiz, L.; Espinosa-Díez, C.; Fernández-Hernando, C.; Kavanagh, T.J.; Lamas, S. The Role of Micrornas in Environmental Risk Factors, Noise-Induced Hearing Loss, and Mental Stress. Antioxid Redox. Signal. 2018, 28, 773–796.
  21. McAllister, J.M.; Han, A.X.; Modi, B.; Teves, M.E.; Mavodza, G.R.; Anderson, Z.L.; Shen, T.; Christenson, L.K.; Archer, K.J.; Strauss, J.F. Mirna Profiling Reveals Mirna-130b-3p Mediates Dennd1a Variant 2 Expression and Androgen Biosynthesis. Endocrinology 2019, 160, 1964–1981.
  22. Dong, H.; Curran, I.; Williams, A.; Bondy, G.; Yauk, C.L.; Wade, M.G. Hepatic Mirna Profiles and Thyroid Hormone Homeostasis in Rats Exposed to Dietary Potassium Perfluorooctanesulfonate (Pfos). Environ. Toxicol. Pharmacol. 2016, 41, 201–210.
  23. Wang, X.; Yang, L.; Wang, H.; Shao, F.; Yu, J.; Jiang, H.; Han, Y.; Gong, D.; Gu, Z. Growth Hormone-Regulated Mrnas and Mirnas in Chicken Hepatocytes. PLoS ONE 2014, 9, e112896.
  24. Aliberti, P.; Sethi, R.; Belgorosky, A.; Chandran, U.R.; Plant, T.M.; Walker, W.H. Gonadotrophin-Mediated Mirna Expression in Testis at Onset of Puberty in Rhesus Monkey: Predictions on Regulation of Thyroid Hormone Activity and Dlk1-Dio3 Locus. Mol. Hum. Reprod. 2019, 25, 124–136.
  25. Tilghman, S.L.; Bratton, M.R.; Segar, H.C.; Martin, E.C.; Rhodes, L.V.; Li, M.; McLachlan, J.A.; Wiese, T.E.; Nephew, K.P.; Burow, M.E. Endocrine Disruptor Regulation of Microrna Expression in Breast Carcinoma Cells. PLoS ONE 2012, 7, e32754.
  26. Meruvu, S.; Zhang, J.; Choudhury, M. Mono-(2-Ethylhexyl) Phthalate Increases Oxidative Stress Responsive Mirnas in First Trimester Placental Cell Line Htr8/Svneo. Chem. Res. Toxicol. 2016, 29, 430–435.
  27. Meruvu, S.; Zhang, J.; Choudhury, M. Butyl Benzyl Phthalate Promotes Adipogenesis in 3t3-L1 Cells Via the Mirna-34a-5p Signaling Pathway in the Absence of Exogenous Adipogenic Stimuli. Chem. Res. Toxicol. 2021, 34, 2251–2260.
  28. Lo, W.-Y.; Peng, C.-T.; Wang, H.-J. Microrna-146a-5p Mediates High Glucose-Induced Endothelial Inflammation Via Targeting Interleukin-1 Receptor-Associated Kinase 1 Expression. Front Physiol. 2017, 8, 551.
  29. Gao, G.-Z.; Zhao, Y.; Li, H.-X.; Li, W. Bisphenol a-Elicited Mir-146a-5p Impairs Murine Testicular Steroidogenesis through Negative Regulation of Mta3 Signaling. Biochem. Biophys. Res. Commun. 2018, 501, 478–485.
  30. Larocca, J.; Binder, A.M.; Mcelrath, T.F.; Michels, K.B. First-Trimester Urine Concentrations of Phthalate Metabolites and Phenols and Placenta Mirna Expression in a Cohort of Us Women. Environ. Health Perspect. 2016, 124, 380–387.
  31. Park, M.H.; Gutiérrez-García, A.K.; Choudhury, M. Mono-(2-Ethylhexyl) Phthalate Aggravates Inflammatory Response Via Sirtuin Regulation and Inflammasome Activation in Raw 264.7 Cells. Chem. Res. Toxicol. 2019, 32, 935–942.
  32. Hanieh, H.; Alzahrani, A. Microrna-132 Suppresses Autoimmune Encephalomyelitis by Inducing Cholinergic Anti-Inflammation: A New Ahr-Based Exploration. Eur. J. Immunol. 2013, 43, 2771–2782.
  33. Guida, M.; Marra, M.; Zullo, F.; Guida, M.; Trifuoggi, M.; Biffali, E.; Borra, M.; De Mieri, G.; D’Alessandro, R.; De Felice, B. Association between Exposure to Dioxin-Like Polychlorinated Biphenyls and Mir-191 Expression in Human Peripheral Blood Mononuclear Cells. Mutat. Res. 2013, 753, 36–41.
  34. Li, G.; Chang, H.; Xia, W.; Mao, Z.; Li, Y.; Xu, S. F0 Maternal Bpa Exposure Induced Glucose Intolerance of F2 Generation through DNA Methylation Change in Gck. Toxicol. Lett. 2014, 228, 192–199.
  35. Skinner, M.K.; Manikkam, M.; Tracey, R.; Guerrero-Bosagna, C.; Haque, M.; Nilsson, E.E. Ancestral Dichlorodiphenyltrichloroethane (Ddt) Exposure Promotes Epigenetic Transgenerational Inheritance of Obesity. BMC Med. 2013, 11, 228.
  36. Crews, D.; Mclachlan, J.A. Epigenetics, Evolution, Endocrine Disruption, Health, and Disease. Endocrinology 2006, 147 (Suppl. 6), S4–S10.
  37. Kaur, S.; Kinkade, J.A.; Green, M.T.; Martin, R.E.; Willemse, T.E.; Bivens, N.J.; Schenk, A.K.; Helferich, W.G.; Trainor, B.C.; Fass, J.; et al. Disruption of Global Hypothalamic Microrna (Mir) Profiles and Associated Behavioral Changes in California Mice (Peromyscus Californicus) Developmentally Exposed to Endocrine Disrupting Chemicals. Horm. Behav. 2021, 128, 104890.
  38. Brevik, A.; Lindeman, B.; Brunborg, G.; Duale, N. Paternal BenzoPyrene Exposure Modulates Microrna Expression Patterns in the Developing Mouse Embryo. Int. J. Cell Biol. 2012, 2012, 407431.
  39. Veiga-Lopez, A.; Luense, L.J.; Christenson, L.K.; Padmanabhan, V. Developmental Programming: Gestational Bisphenol-a Treatment Alters Trajectory of Fetal Ovarian Gene Expression. Endocrinology 2013, 154, 1873–1884.
  40. Brieño-Enríquez, M.A.; García-López, J.; Cárdenas, D.B.; Guibert, S.; Cleroux, E.; Děd, L.; Hourcade, J.D.D.; Pěknicová, J.; Weber, M.; del Mazo, J. Exposure to Endocrine Disruptor Induces Transgenerational Epigenetic Deregulation of Micrornas in Primordial Germ Cells. PLoS ONE 2015, 10, e0124296.
  41. Fullston, T.; Teague, E.M.C.O.; Palmer, N.O.; DeBlasio, M.J.; Mitchell, M.; Corbett, M.; Print, C.G.; Owens, J.A.; Lane, M. Paternal Obesity Initiates Metabolic Disturbances in Two Generations of Mice with Incomplete Penetrance to the F2 Generation and Alters the Transcriptional Profile of Testis and Sperm Microrna Content. Faseb. J. 2013, 27, 4226–4243.
  42. Ho, S.-M.; Cheong, A.; Adgent, M.A.; Veevers, J.; Suen, A.A.; Tam, N.N.C.; Leung, Y.-K.; Jefferson, W.N.; Williams, C.J. Environmental Factors, Epigenetics, and Developmental Origin of Reproductive Disorders. Reprod. Toxicol. 2017, 68, 85–104.
  43. Kelly, T.L.; Trasler, J.M. Reproductive Epigenetics. Clin. Genet. 2004, 65, 247–260.
  44. Bredfeldt, T.G.; Greathouse, K.L.; Safe, S.H.; Hung, M.C.; Bedford, M.T.; Walker, C.L. Xenoestrogen-Induced Regulation of Ezh2 and Histone Methylation Via Estrogen Receptor Signaling to Pi3k/Akt. Mol Endocrinol. 2010, 24, 993–1006.
  45. Ma, J.-Y.; Li, M.; Ge, Z.-J.; Luo, Y.; Ou, X.-H.; Song, S.; Tian, D.; Yang, J.; Zhang, B.; Ou-Yang, Y.-C.; et al. Whole Transcriptome Analysis of the Effects of Type I Diabetes on Mouse Oocytes. PLoS ONE 2012, 7, e41981.
  46. Yang, C.; Song, G.; Lim, W. A Mechanism for the Effect of Endocrine Disrupting Chemicals on Placentation. Chemosphere 2019, 231, 326–336.
  47. Chen, C.Y.; Chen, C.P.; Lin, K.H. Biological Functions of Thyroid Hormone in Placenta. Int. J. Mol. Sci. 2015, 16, 4161–4179.
  48. Zoeller, R.T. Endocrine Disrupting Chemicals and Thyroid Hormone Action. Adv. Pharmacol. 2021, 92, 401–417.
  49. Aranda, A. Micrornas and Thyroid Hormone Action. Mol. Cell Endocrinol. 2021, 525, 111175.
  50. Lin, Y.-H.; Wu, M.-H.; Liao, C.-J.; Huang, Y.-H.; Chi, H.-C.; Wu, S.-M.; Chen, C.-Y.; Tseng, Y.-H.; Tsai, C.-Y.; Chung, I.-H.; et al. Repression of Microrna-130b by Thyroid Hormone Enhances Cell Motility. J. Hepatol. 2015, 62, 1328–1340.
  51. Jazdzewski, K.; Boguslawska, J.; Jendrzejewski, J.; Liyanarachchi, S.; Pachucki, J.; Wardyn, K.A.; Nauman, A.; de la Chapelle, A. Thyroid Hormone Receptor B (Thrb) Is a Major Target Gene for Micrornas Deregulated in Papillary Thyroid Carcinoma (Ptc). J. Clin. Endocrinol. Metab. 2011, 96, E546–E553.
  52. Yu, Z.; Han, Y.; Shen, R.; Huang, K.; Xu, Y.-Y.; Wang, Q.-N.; Zhou, S.-S.; Xu, D.-X.; Tao, F.-B. Gestational Di-(2-Ethylhexyl) Phthalate Exposure Causes Fetal Intrauterine Growth Restriction through Disturbing Placental Thyroid Hormone Receptor Signaling. Toxicol. Lett. 2018, 294, 1–10.
  53. Berlin, M.; Barchel, D.; Brik, A.; Kohn, E.; Livne, A.; Keidar, R.; Tovbin, J.; Betser, M.; Moskovich, M.; Mandel, D.; et al. Maternal and Newborn Thyroid Hormone, and the Association with Polychlorinated Biphenyls (Pcbs) Burden: The Ehf (Environmental Health Fund) Birth Cohort. Front Pediatr. 2021, 9, 705395.
  54. Avissar-Whiting, M.; Veiga, K.R.; Uhl, K.M.; Maccani, M.A.; Gagne, L.A.; Moen, E.L.; Marsit, C.J. Bisphenol a Exposure Leads to Specific Microrna Alterations in Placental Cells. Reprod. Toxicol. 2010, 29, 401–406.
  55. Wang, X.K.; Agarwal, M.; Parobchak, N.; Rosen, A.; Vetrano, A.M.; Srinivasan, A.; Wang, B.; Rosen, T. Mono-(2-Ethylhexyl) Phthalate Promotes Pro-Labor Gene Expression in the Human Placenta. PLoS ONE 2016, 11, e0147013.
  56. Shoaito, H.; Petit, J.; Chissey, A.; Auzeil, N.; Guibourdenche, J.; Gil, S.; Laprévote, O.; Fournier, T.; Degrelle, S.A. The Role of Peroxisome Proliferator–Activated Receptor Gamma (Pparγ) in Mono(2-Ethylhexyl) Phthalate (Mehp)-Mediated Cytotrophoblast Differentiation. Environ. Health Perspect. 2019, 127, 27003.
  57. Petit, J.; Wakx, A.; Gil, S.; Fournier, T.; Auzeil, N.; Rat, P.; Laprévote, O. Lipidome-Wide Disturbances of Human Placental Jeg-3 Cells by the Presence of Mehp. Biochimie 2018, 149, 1–8.
  58. De Felice, B.; Manfellotto, F.; Palumbo, A.R.; Troisi, J.; Zullo, F.; Di Carlo, C.; Sardo, A.D.S.; De Stefano, N.; Ferbo, U.; Guida, M.; et al. Genome-Wide Microrna Expression Profiling in Placentas from Pregnant Women Exposed to Bpa. BMC Med. Genom. 2015, 8, 56.
  59. Vizcaino, E.; Grimalt, J.O.; Fernández-Somoano, A.; Tardon, A. Transport of Persistent Organic Pollutants across the Human Placenta. Environ. Int. 2014, 65, 107–115.
  60. Cariou, R.; Veyrand, B.; Yamada, A.; Berrebi, A.; Zalko, D.; Durand, S.; Pollono, C.; Marchand, P.; Leblanc, J.-C.; Antignac, J.-P.; et al. Perfluoroalkyl Acid (Pfaa) Levels and Profiles in Breast Milk, Maternal and Cord Serum of French Women and Their Newborns. Environ. Int. 2015, 84, 71–81.
  61. Mørck, T.J.; Sorda, G.; Bechi, N.; Rasmussen, B.S.; Nielsen, J.B.; Ietta, F.; Rytting, E.; Mathiesen, L.; Paulesu, L.; Knudsen, L.E. Placental Transport and in Vitro Effects of Bisphenol A. Reprod. Toxicol. 2010, 30, 131–137.
  62. Stefanidou, M.; Maravelias, C.; Spiliopoulou, C. Human Exposure to Endocrine Disruptors and Breast Milk. Endocr. Metab. Immune Disord Drug Targets 2009, 9, 269–276.
  63. Chang, G.; Mouillet, J.-F.; Mishima, T.; Chu, T.; Sadovsky, E.; Coyne, C.B.; Parks, W.T.; Surti, U.; Sadovsky, Y. Expression and Trafficking of Placental Micrornas at the Feto-Maternal Interface. FASEB J. 2017, 31, 2760–2770.
  64. Tsitsiou, E.; Lindsay, M.A. Micrornas and the Immune Response. Curr. Opin Pharm. 2009, 9, 514–520.
  65. Perry, M.M.; Moschos, S.A.; Williams, A.E.; Shepherd, N.J.; Larner-Svensson, H.M.; Lindsay, M.A. Rapid Changes in Microrna-146a Expression Negatively Regulate the Il-1beta-Induced Inflammatory Response in Human Lung Alveolar Epithelial Cells. J. Immunol. 2008, 180, 5689–5698.
  66. He, Y.; Sun, X.; Huang, C.; Long, X.-R.; Lin, X.; Zhang, L.; Lv, X.-W.; Li, J. Mir-146a Regulates Il-6 Production in Lipopolysaccharide-Induced Raw264.7 Macrophage Cells by Inhibiting Notch1. Inflammation 2014, 37, 71–82.
  67. Lorente-Cebrián, S.; Mejhert, N.; Kulyté, A.; Laurencikiene, J.; Åström, G.; Hedén, P.; Ryden, M.; Arner, P. Micrornas Regulate Human Adipocyte Lipolysis: Effects of Mir-145 Are Linked to Tnf-A. PLoS ONE 2014, 9, e86800.
  68. Tili, E.; Michaille, J.J.; Cimino, A.; Costinean, S.; Dumitru, C.D.; Adair, B.; Fabbri, M.; Alder, H.; Liu, C.G.; Calin, G.A.; et al. Modulation of Mir-155 and Mir-125b Levels Following Lipopolysaccharide/Tnf-Alpha Stimulation and Their Possible Roles in Regulating the Response to Endotoxin Shock. J. Immunol. 2007, 179, 5082–5089.
  69. Imaizumi, T.; Tanaka, H.; Tajima, A.; Yokono, Y.; Matsumiya, T.; Yoshida, H.; Tsuruga, K.; Aizawa-Yashiro, T.; Hayakari, R.; Inoue, I.; et al. Ifn-Γ and Tnf-A Synergistically Induce Microrna-155 Which Regulates Tab2/Ip-10 Expression in Human Mesangial Cells. Am. J. Nephrol. 2010, 32, 462–468.
  70. Xie, Y.F.; Shu, R.; Jiang, S.Y.; Liu, D.L.; Ni, J.; Zhang, X.L. Microrna-146 Inhibits Pro-Inflammatory Cytokine Secretion through Il-1 Receptor-Associated Kinase 1 in Human Gingival Fibroblasts. J. Inflamm. 2013, 10, 20.
  71. Doberstein, K.; Steinmeyer, N.; Hartmetz, A.-K.; Eberhardt, W.; Mittelbronn, M.; Harter, P.N.; Juengel, E.; Blaheta, R.; Pfeilschifter, J.; Gutwein, P. Microrna-145 Targets the Metalloprotease Adam17 and Is Suppressed in Renal Cell Carcinoma Patients. Neoplasia 2013, 15, 218–230.
  72. Liu, Y.C.; Zou, X.B.; Chai, Y.F.; Yao, Y.M. Macrophage Polarization in Inflammatory Diseases. Int. J. Biol. Sci. 2014, 10, 520–529.
  73. Essandoh, K.; Li, Y.; Huo, J.; Fan, G.C. Mirna-Mediated Macrophage Polarization and Its Potential Role in the Regulation of Inflammatory Response. Shock 2016, 46, 122–131.
  74. Curtale, G.; Mirolo, M.; Renzi, T.A.; Rossato, M.; Bazzoni, F.; Locati, M. Negative Regulation of Toll-Like Receptor 4 Signaling by Il-10-Dependent Microrna-146b. Proc. Natl. Acad. Sci. USA 2013, 110, 11499–11504.
  75. Ban, E.; Jeong, S.; Park, M.; Kwon, H.; Park, J.; Song, E.J.; Kim, A. Accelerated Wound Healing in Diabetic Mice by Mirna-497 and Its Anti-Inflammatory Activity. Biomed. Pharm. 2020, 121, 109613.
  76. Gordon, S.; Taylor, P.R. Monocyte and Macrophage Heterogeneity. Nat. Rev. Immunol. 2005, 5, 953–964.
  77. Mantovani, A.; Biswas, S.K.; Galdiero, M.R.; Sica, A.; Locati, M. Macrophage Plasticity and Polarization in Tissue Repair and Remodelling. J. Pathol. 2013, 229, 176–185.
  78. Ginhoux, F.; Greter, M.; Leboeuf, M.; Nandi, S.; See, P.; Gokhan, S.; Mehler, M.F.; Conway, S.J.; Ng, L.G.; Stanley, E.R.; et al. Fate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages. Science 2010, 330, 841–845.
  79. Hoeffel, G.; Wang, Y.; Greter, M.; See, P.; Teo, P.; Malleret, B.; Leboeuf, M.; Low, D.; Oller, G.; Almeida, F.; et al. Adult Langerhans Cells Derive Predominantly from Embryonic Fetal Liver Monocytes with a Minor Contribution of Yolk Sac–Derived Macrophages. J. Exp. Med. 2012, 209, 1167–1181.
  80. Luinenburg, D.G.; De Haan, G. Micrornas in Hematopoietic Stem Cell Aging. Mech. Ageing Dev. 2020, 189, 111281.
  81. Lazare, S.S.; Wojtowicz, E.E.; Bystrykh, L.V.; De Haan, G. Micrornas in Hematopoiesis. Exp. Cell. Res. 2014, 329, 234–238.
  82. Gerrits, A.; Walasek, M.A.; Olthof, S.; Weersing, E.; Ritsema, M.; Zwart, E.; Van Os, R.; Bystrykh, L.V.; de Haan, G. Genetic Screen Identifies Microrna Cluster 99b/Let-7e/125a as a Regulator of Primitive Hematopoietic Cells. Blood 2012, 119, 377–387.
  83. Lechman, E.R.; Gentner, B.; van Galen, P.; Giustacchini, A.; Saini, M.; Boccalatte, F.E.; Hiramatsu, H.; Restuccia, U.; Bachi, A.; Voisin, V.; et al. Attenuation of Mir-126 Activity Expands Hsc in Vivo without Exhaustion. Cell. Stem. Cell. 2012, 11, 799–811.
  84. Lechman, E.R.; Gentner, B.; Ng, S.W.; Schoof, E.M.; van Galen, P.; Kennedy, J.A.; Nucera, S.; Ciceri, F.; Kaufmann, K.B.; Takayama, N.; et al. Mir-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells. Cancer Cell 2016, 29, 214–228.
  85. Starczynowski, D.T.; Kuchenbauer, F.; Argiropoulos, B.; Sung, S.; Morin, R.; Muranyi, A.; Hirst, M.; Hogge, D.; Marra, M.; Wells, R.A.; et al. Identification of Mir-145 and Mir-146a as Mediators of the 5q- Syndrome Phenotype. Nat. Med. 2010, 16, 49–58.
  86. Guo, S.; Lu, J.; Schlanger, R.; Zhang, H.; Wang, J.Y.; Fox, M.C.; Purton, L.E.; Fleming, H.H.; Cobb, B.; Merkenschlager, M.; et al. Microrna Mir-125a Controls Hematopoietic Stem Cell Number. Proc. Natl. Acad. Sci. USA 2010, 107, 14229–14234.
  87. Bowers, E.; Singer, K. Obesity-Induced Inflammation: The Impact of the Hematopoietic Stem Cell Niche. JCI Insight. 2021, 6, e145295.
  88. Vinci, M.C.; Gambini, E.; Bassetti, B.; Genovese, S.; Pompilio, G. When Good Guys Turn Bad: Bone Marrow’s and Hematopoietic Stem Cells’ Role in the Pathobiology of Diabetic Complications. Int. J. Mol. Sci. 2020, 21, 3864.
  89. Pospisil, V.; Vargova, K.S.; Kokavec, J.; Rybarova, J.; Savvulidi, F.G.; Jonasova, A.; Nečas, E.; Zavadil, J.; Laslo, P.; Stopka, T. Epigenetic Silencing of the Oncogenic Mir-17-92 Cluster During Pu.1-Directed Macrophage Differentiation. Embo. J. 2011, 30, 4450–4464.
  90. Berg, S.M.; Seijkens, T.T.P.; Kusters, P.J.H.; Beckers, L.; Toom, M.; Smeets, E.; Levels, J.; Winther, M.P.J.; Lutgens, E. Diet-Induced Obesity in Mice Diminishes Hematopoietic Stem and Progenitor Cells in the Bone Marrow. Faseb. J. 2016, 30, 1779–1788.
  91. Lee, J.-M.; Govindarajah, V.; Goddard, B.; Hinge, A.; Muench, D.E.; Filippi, M.-D.; Aronow, B.; Cancelas, J.A.; Salomonis, N.; Grimes, H.L.; et al. Obesity Alters the Long-Term Fitness of the Hematopoietic Stem Cell Compartment through Modulation of Gfi1 Expression. J. Exp. Med. 2018, 215, 627–644.
  92. Wynn, T.A.; Chawla, A.; Pollard, J.W. Macrophage Biology in Development, Homeostasis and Disease. Nature 2013, 496, 445–455.
  93. Caescu, C.I.; Guo, X.; Tesfa, L.; Bhagat, T.D.; Verma, A.; Zheng, D.; Stanley, E.R. Colony Stimulating Factor-1 Receptor Signaling Networks Inhibit Mouse Macrophage Inflammatory Responses by Induction of Microrna-21. Blood 2015, 125, e1–e13.
  94. Lafontan, M. Fat Cells: Afferent and Efferent Messages Define New Approaches to Treat Obesity. Annu. Rev. Pharmacol. Toxicol. 2005, 45, 119–146.
  95. Longo, M.; Zatterale, F.; Naderi, J.; Parrillo, L.; Formisano, P.; Raciti, G.A.; Beguinot, F.; Miele, C. Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications. Int. J. Mol. Sci. 2019, 20, 2538.
  96. Yan, X.; Huang, Y.; Zhao, J.-X.; Rogers, C.J.; Zhu, M.-J.; Ford, S.P.; Nathanielsz, P.W.; Du, M. Maternal Obesity Downregulates Microrna Let-7g Expression, a Possible Mechanism for Enhanced Adipogenesis During Ovine Fetal Skeletal Muscle Development. Int. J. Obes. 2013, 37, 568–575.
  97. Yasmin, F.; Sahito, A.M.; Mir, S.L.; Khatri, G.; Shaikh, S.; Gul, A.; Hassan, S.A.; Koritala, T.; Surani, S. Electrical Neuromodulation Therapy for Inflammatory Bowel Disease. World J. Gastrointest Pathophysiol. 2022, 13, 128–142.
  98. Wang, J.; Long, R.; Han, Y. The Role of Exosomes in the Tumour Microenvironment on Macrophage Polarisation. Biochim. Biophys Acta. Rev. Cancer. 2022, 1877, 188811.
  99. Ghafouri-Fard, S.; Niazi, V.; Taheri, M. Role of Mirnas and Lncrnas in Hematopoietic Stem Cell Differentiation. Noncoding RNA Res. 2021, 6, 8–14.
  100. Chu, A.J.; Williams, J.M. Astrocytic Microrna in Ageing, Inflammation, and Neurodegenerative Disease. Front. Physiol. 2021, 12, 826697.
  101. Liu, S.; Ren, C.; Qu, X.; Wu, X.; Dong, F.; Chand, Y.K.; Fan, H.; Yao, R.; Geng, D. Mir-219 Attenuates Demyelination in Cuprizone-Induced Demyelinated Mice by Regulating Monocarboxylate Transporter 1. Eur. J. Neurosci. 2017, 45, 249–259.
  102. Krug, A.; Wöhr, M.; Seffer, D.; Rippberger, H.; Sungur, A.; Dietsche, B.; Stein, F.; Sivalingam, S.; Forstner, A.J.; Witt, S.H.; et al. Advanced Paternal Age as a Risk Factor for Neurodevelopmental Disorders: A Translational Study. Mol. Autism. 2020, 11, 54.
  103. Rodriguez-Gomez, A.; Filice, F.; Gotti, S.; Panzica, G. Perinatal Exposure to Genistein Affects the Normal Development of Anxiety and Aggressive Behaviors and Nitric Oxide System in Cd1 Male Mice. Physiol. Behav. 2014, 133, 107–114.
  104. Marraudino, M.; Ponti, G.; Moussu, C.; Farinetti, A.; Macchi, E.; Accornero, P.; Gotti, S.; Collado, P.; Keller, M.; Panzica, G. Early Postnatal Genistein Administration Affects Mice Metabolism and Reproduction in a Sexually Dimorphic Way. Metabolites 2021, 11, 449.
  105. Zhou, P.; Wu, S.; Huang, D.; Wang, K.; Su, X.; Yang, R.; Shao, C.; Wu, J. Oral Exposure to Dehp May Stimulate Prostatic Hyperplasia Associated with Upregulation of Cox-2 and L-Pgds Expressions in Male Adult Rats. Reprod. Toxicol. 2022, 112, 160–170.
  106. Singh, V.; Cortes-Ramirez, J.; Toms, L.M.; Sooriyagoda, T.; Karatela, S. Effects of Polybrominated Diphenyl Ethers on Hormonal and Reproductive Health in E-Waste-Exposed Population: A Systematic Review. Int. J. Environ. Res. Public Health 2022, 19, 7820.
  107. Chen, S.-D.; Sun, X.-Y.; Niu, W.; Kong, L.-M.; He, M.-J.; Fan, H.-M.; Li, W.-S.; Zhong, A.-F.; Zhang, L.-Y.; Lu, J. Correlation between the Level of Microrna Expression in Peripheral Blood Mononuclear Cells and Symptomatology in Patients with Generalized Anxiety Disorder. Compr. Psychiatry 2016, 69, 216–224.
More
Information
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : , , ,
View Times: 294
Revisions: 2 times (View History)
Update Date: 11 Nov 2022
1000/1000
Video Production Service