Astroglial sncRNA Relevance on Early Neurodegeneration Stages: History
Please note this is an old version of this entry, which may differ significantly from the current revision.

Astrocyte dysfunction with consequential neuronal microenvironment dysregulation (astrocytopathy) has been involved in processes of early neurodegenerative disease. Small non-coding RNA (sncRNA) vary in different detrimental conditions of Central Nervous System (CNS), and sustained changes in sncRNA astrocyte expression profile can be the consequence of these conditions. sncRNA signatures derived from astrocytes, could therefore be a key to reveal early neurodegenerative disease, helping to unravel the astrocyte role in neurodegenerative disease. Current biomarkers for neurodegenerative disease, face strong challenges such as high variability, negative cost-effectiveness, low availability, or invasiveness. For example, cerebrospinal fluid evaluation (CSF tests) is a highly invasive, expensive, risky procedure, often used in the diagnosis of neurodegenerative disease. The alternative to CSF tests, which is neuroimaging requires especial equipment, long operating time and it is highly expensive making their widespread use prohibitive. Still, misdiagnosis could occur after the use of these powerful tools. Therefore, new methods are needed to assess neurodegeneration, and extracellular vesicles from astrocytes (ADEV) represent and interesting target of research. ADEV cross blood brain-barrier (BBB) carrying sncRNA from astrocytes and cell-specific membrane surface proteins, which can be used to allow ADEV separation from vesicles of other sources and other contaminants. This approach could be useful for the analysis of a less invasive, simpler, peripheral sample of blood origin. sncRNA dysregulated in conditions associated with increased risk of neurodegenerative disease and their possible effects on target cells is shown.

  • Astrocyte Derived Extracellular Vesicles (ADEVs)
  • small non-coding RNA (sncRNA)
  • sncRNA transcriptome (sncRNome)
  • circulating sncRNA
  • extracellular sncRNA

1. Introduction

Neurodegenerative diseases are caused by a general dysfunction of the Central Nervous System (CNS), characterized by progressive loss of neuron structure and function[1]. In recent years, neurodegenerative diseases have become a global public health problem due in part to the increase in the elderly population in both developed and under developing countries. Pathologies such as Alzheimer’s disease (49–65%) [2][3], Parkinson’s disease (15%) [2], Vascular Dementia and Multiple Sclerosis, among others, are included within the ND. Environmental factors play an essential role in the etiology of neurodegenerative diseases and sporadic origin is dominant; vascular dementia is an acquired disease, and sporadic cases represent more than 95% of Alzheimer’s disease, 90% of Parkinson’s disease and 80% of Multiple Sclerosis [4][5][6]. Diagnosis of neurodegenerative diseases is made difficult by lack of precision and it is based in the analysis of clinical history (mainly through cognitive and motor neurological examination) [7][8], and paraclinical assessment that includes neuroimaging, and Cerebrospinal Fluid (CSF) evaluation [8][9][10]. Clinical assessment depends on symptoms, often not so apparent [7], and often it is prone to bias and lack of accuracy.

Another characteristic of neurodegenerative diseases diagnosis is the complexity associated with paraclinical assessment which troubles timely diagnosis. Detection of distinct hallmarks of neurodegenerative diseases has been possible with neuroimaging and CSF evaluation up to very early time points before symptoms onset (~30 years) [11]. However, invasiveness, low availability, and risk associated with CSF measures [11], and high costs, long operating time, and inaccessibility associated with neuroimaging [8][12], limits the widespread use of these markers. Moreover, the presence of this alterations is not enough for diagnosis. Such a situation limits the success and the extent of therapies and treatments [11][13][14][15], but it is also an opportunity for simpler peripheral biomarkers which are preferred due to their lower invasiveness, risk, and complexity [16]. In support of this view successful CSF or neuroimaging biomarkers have been evaluated in peripheral fluids such as blood, saliva, plasma, serum, and tears, but markers showing promising results in CSF and neuroimaging require ultrasensitive techniques for peripheral evaluation due to reduced concentration and cross-reactivities [8]. Still with biosensor detection down to femtomolar levels [17], fluctuations non associated with disease also affect biomarker performance [18][19][20]. Recently, composite measurements of biomarkers (e.g., t-tau/Aβ42, p-tau/Aβ42, Aβ42/Aβ40) have improved the precision of peripheral based biomarkers[17], but there remains an urgency for the development of simpler cost-effective biomarkers for the detection of neurodegenerative diseases in early neurodegeneration stages [11][15].

Astrocytes regulate central processes for neuronal microenvironment maintenance, protection, and repair [21][22], including neuroinflammation [23], which is a hallmark in most neurodegenerative deseases. Depending on severity or duration an insult/injury can lead to astrocyte dysfunction either by impairment of the normal process or by gain of an abnormal function (astrogliosis), which could trigger neurodegeneration by neuronal microenvironment dysregulation (a process termed astrocytopathy) [24]. Astroglial pathology has been detected before symptoms onset in various neurodegenerative diseases [25][26][27]. Hence astrocyte dysfunction constitutes a target for early neurodegeneration biomarker research. A variety of glial-derived substances such as DJ-1, CCL2, CCL7, CXCL10, interleukins (IL-1β, IL-2, IL-6, IL-8, IL-12, IL-18), and CRP [16][28] have been studied with diagnostic interest. Interestingly some of them have shown diagnostic potential in peripheral tissues such as plasma for Alzheimer’s disease or tears for Parkinson’s disease [16][28], and it is likely that these testing become routine screening target for neurodegenerative diseases early diagnosis.

2. Astrocyte Relevance on Early Neurodegeneration Stages

Neurodegenerative disease (ND) etiology is particularly difficult to define, for instance Aβ peptides, which are the most representative hallmark of Alzheimer’s disease, have been observed to reduce oxidative stress in some circumstances, blurring the limits between pathological and physiological changes [29], therefore neurodegenerative diseases onset is highly heterogeneous, undefined, and not well understood [30], and early phases of neurodegenerative diseases difficult to define. Early neurodegeneration stages can be defined in two well separate phases that vary between diseases: preclinical and prodromal [7][20][30]. Preclinical phases can be further partitioned in pre-symptomatic and early symptomatic, while the prodromal stage is characterized by symptoms not strong enough to consider a diagnosis but clearly evidenced in clinical settings [11]. Astrocyte dysfunction appears in early phases of Alzheimer’s disease, and early Parkinson’s disease (<5 years of disease), as imaged in vivo by positron emission tomography (PET) of 11C-deuterium-L-deprenyl (11C-DED) and 11C-BU99008, respectively both of which recognize reactive astrocytes [31][32]. 11C-DED has been observed in mild cognitive impairment [31], and the astrocytic enzyme targeted by this ligand which is monoamine oxidase B (MAO-B) is a promissory biomarker in Multiple Sclerosis [32]. Therefore, astrocyte dysfunction biomarkers should identify early neurodegeneration stages in most neurodegenerative diseases before extensive neuronal damage occurs.

Astrocytes perform multifold functions some of them essential such as regulating electrochemical balance, distributing the energy uptake (meeting the high energy requirement of neurons), and accelerating detoxification which protect neurons from oxidative damage [22]. Several papers summarize astrocyte general functions and in specific contexts such as innate immunity, inflammation, and neuroprotection [21][33][34][35][36]. Astrocytes respond to CNS injury/lesion with the activation of a complex heterogenous response termed astrogliosis [24], which can lead to the activation of pivotal processes for neurodegenerative diseases such as neuroinflammation. Since astrogliosis modifies astrocytic function (sometimes permanently), neurodegeneration can start because of both, the reduction of essential functions performed by astrocytes and an exacerbated astrocytic activity (abnormal gain of function), this is formally called astrocytophaty [24]. Growing evidence supports that astrocyte dysfunction is sufficient by itself to start secondary neurodegenerative process in early neurodegenerative stages of different neurodegenerative diseases.

For instance, in Alzheimer Disease abnormal astrocyte exposure to saturated fatty acids such as stearic, linoleic, oleic and palmitic acid has been linked with higher risk [37][38]. High exposures of human astrocytes to palmitic acid decreased cell viability and mitochondrial membrane potential, also producing autophagy impairment, proinflammatory cytokine overproduction (IL-1β, IL-6 and TNF-α), endoplasmic reticulum stress, and morphological changes associated with dysfunction [39][40][41]. Furthermore, neuron exposition to equivalent concentrations of palmitic acid did not generate the same effect [38][42], but when neurons were exposed to media from astrocytes induced with palmitic acid toxicity, hyperphosphorylation of tau [38], and induction of Aβ peptide production was observed [43]. Both marks associate with onset of Alzheimer’s disease and appear in early neurodegeneration stages [11][44].

Animal models and human also support in vitro observations situating astrocyte dysfunction as an early pathological event in Alzheimer’s disease. In animal models, High Fat Diet robustly induced cognitive impairment in healthy rat [45] and Tg2576 mouse mutant APP model of Alzheimer’s disease [46]. Tg2576 mouse also showed higher production of amyloidogenic Aβ peptides and higher γ secretase activity after High Fat Diet [46], as well as some contradictory results with improved cognitive functions and no Aβ significant burden in some studies [47]. Alterations in the fatty acid composition seem to be responsible for these contradictions [47] but sex differences could be also responsible because study with contradictory results did not account for animal sex [47]. In general, metabolic disorder models (including High Fat Diet) caused alterations in neuroinflammation and BBB function (processes key controlled by astrocytes) in both animal models (including zebra fish) and humans [48]. Lastly, high-glycemic-load diet exposure of healthy humans caused higher Aβ burden measured by PET and an increasing saturated fatty acids concentration associated with progression to Alzheimer’s disease in human serum and brain tissue [37], therefore helping to explain relationship between dyslipidemia and related metabolic disorders with Alzheimer’s disease and recapitulating in vitro observations.

Parkinson’s Disease development is partly due to astrocyte dysfunction with evidence building up to suggest early astroglial participation in neuroinflammation and in the disruption of several neuroprotective mechanisms as partly initiator events [49]. Several of the 19 genes causative genes of mendelian forms of Parkinson’s disease, express in equal amount in astrocytes than in neurons, with GBA, EIF4G1, VPS35, FBXO7 and PINK1, showing higher expression in astrocytes than in neurons [49][50]. Mutations of these genes in astrocytes have been shown to disrupt lipid metabolism, proliferation, glutamate uptake, cytokine regulation, neurotrophic signaling, anti-inflammatory secretion, and therefore a role in early phases of disease is possible [49]. Animal models of Parkinson’s disease have also shown increased expression of GFAP, neuroinflammation and onset of astrogliosis before motor symptoms [49][51]. Induced by neurotoxin 6-hydroxydopamine and rotenone Parkinson’s disease models also displayed earlier neurodegeneration and neuroprotection diminishment concomitant with astroglial dysfunction in astrocyte conditional mutation [49].

Efforts in Vascular Dementia early detection center in the identification of subclinical symptoms of cerebrovascular conditions that precede this condition, since a stroke constitute a risk marker by itself. Most vascular dementia cases arise after vascular damage caused by smaller and less evident pathophysiological lesions such as lacunar infarct [52]. In most cases such lesions are detected by neuroimaging and therefore there remains cost and accessibility issues for their widespread use, however alternatives of detection such as neurological tests have been proposed [53]. Combined protein detection of CRP, homocysteine and Toll-like receptor 4 (TLR4) in serum have shown biomarker value for cognitive abnormalities related with Cerebral Small Vessel Disease which is the most common vascular abnormality associated with vascular dementia [54]. Evidence shows that these preceding vascular abnormalities induce changes in astrocyte function, including astrocyte activation, end-foot disruption, and EAAT2 and AQP4 downregulation. homocysteine induced vascular dementia mouse model similarly showed astrocytic end-foot disruption concomitant to AQP4 downregulation with astrogial activation, and these astrocytic changes took place in a symptomatic phase (cognitive deficits measured in mice) after microglial activation [52]. This evidence shows that measuring astrocytic functional changes could have a biomarker value in specific stages of vascular dementia with microglial changes being more relevant for early detection, but it requires further research and other models of vascular dementia to confirm these observations.

In Multiple Sclerosis, astrocyte dysfunction takes place before the glial scar formation, previously believed to be the earliest phase in which astrocyte dysfunction took place. Evidence shows that, before lesion demyelination, astrocytes contribute to the inflammatory response that results in the recruitment of lymphocytes and regulate BBB and BSCB permeability to favor lesion [55]. Evidence in preclinical model of experimental autoimmune encephalomyelitis strongly support astrocyte dysfunction role in early phases of Multiple Sclerosis disrupting BBB, BSCB and promoting lymphocyte recruitment. Astrocyte-specific CCL2 deletion (a central gene in BBB disruption) in mouse ameliorated Multiple Sclerosis in experimental autoimmune encephalomyelitis [23][55]. Furthermore lactosylceramide, an activator of CCL2 and powerful inflammatory molecule, is overexpressed in astrocytes of the experimental autoimmune encephalomyelitis model and its inhibition suppressed neurodegeneration [55][56]. In humans, it has been found that genetic risk factors of Multiple Sclerosis cause a strong in vitro probed effect in astrocyte function that increases NF-κB signaling and chemokine liberation, which can be related with lymphocyte recruitment in prodromal stages. In addition, astrocytes perform neuroprotective roles in Multiple Sclerosis such as the recruitment of microglia in damaged myelin clearance to favor lesion repair [55] that may take place in symptomatic phases of the disease.

Several conditions, neurological disorders, and lesions that associates with increased risk of neurodegenerative diseases cause alterations in astrocyte function, which could precede neurodegenerative disease. A proinflammatory microenvironment, oxygen and glucose deprivation, intracerebral hemorrhage, traumatic brain injury, Postoperative Cognitive Dysfunction and ethanol exposure, represent conditions inducing increased risk of neurodegenerative diseases [37][52][57][58][59][60]. Neurovascular unit astrocytes suffer atrophy of end-foot processes under ischemia, traumatic brain injury, brain contusion and neurodegenerative diseases [52][61], while morphine induces neuroinflammation and permanent cognitive deficit in a Postoperative Cognitive Dysfunction rat model [58][60], in which astrocyte mediated activation of microglia possibly initiates the insult [58]. Furthermore, rat models demonstrate Parkinson’s disease -like deficits in motor function after repeated cycles of binge-like ethanol intake [62]. Independently of the origin, astrocyte dysfunction generates changes in their secretory profile, this includes the sncRNA from Astrocyte Derived Extracellular Vesicle (ADEV). This fraction contributes to total extracellular vesicle derived sncRNA, which is the most studied source of extracellular sncRNA that has been evaluated in neurodegenerative diseases [58][63][64][65][66][67]. However, to the researchers' knowledge, there are no studies yet that had separately analyzed individual astrocyte-specific sncRNA signatures in human sample in early neurodegeneration stages. Table 1 shows sncRNA from ADEV found dysregulated in conditions associated with early neurodegeneration and neurodegenerative diseases risk in human, mouse, and rat models. These conditions include Il-1β and TNF-α stimulus [63], Hypoxic-Ischemic Brain Damage [68], ischemic preconditioning [65], SOD1 mutation [69], ethanol induced cell toxicity, and morphine-mediated neuroinflammatory microenvironment which is associated with Postoperative Cognitive Dysfunction [58]. As the table shows, astrocyte-specific circulating sncRNA could change in response to early neurodegenerative processes making early neurodegeneration associated with astrocyte dysfunction identifiable.

Table 1. Astrocyte Derived Extracellular Vesicle (ADEV) derived sncRNA dysregulated in conditions associated with increased risk of neurodegenerative disease (NDD) and their possible effects on cell targets based on evidence in human, as well on rat and mouse models. The third column specifies the change in expression favored by conditions associated with increased risk of NDD. ALS: Amyotrophic lateral sclerosis, ASCI: Acute Spinal Cord Injury, CRC: colorectal cancer, EAE: Experimental Autoimmune Encephalomyelitis, HAND: HIV associated neurocognitive disorders, HFD: High-fat diet, HIBD: Hypoxic-Ischemic Brain Damage, IBZ: Ischemic Boundary Zone, NPC: Neural Progenitor Cells, OSA: Obstructive Sleep Apnea, PASMCs: Pulmonary Artery Smooth Muscle Cells, pMCAO: permanent Mid Cerebral Artery Occlusion, SMA: Spinal Muscular Atrophy, SCI: Spinal Cord Injury, TBI: Traumatic brain Injury.



Role Associated with Early Neurodegeneration Conditions or Risk of Neurodegeneration

Role in Neurodegenerative Disease or Effects in CNS Cells

Additional Roles and Effects in Peripheral Cells


Il-1β stimulation, ischemia

Upregulated in ADEV after Il-1β stimulation in primary rat astrocytes [63], upregulated in rat pMCAO ischemia model after lesion [70]

Sporadic ALS downregulated biomarker [71], upregulated in AD hippocampus [72]. Targets involved in FoxO and MAPK signaling pathways and apoptosis [71]. Increased after HFD in rat [73]. •

Promotes differentiation in rat neural stem cells [74]. Downregulates NDRG3 expression in rat cortical neurons to regulate hypoxia response (proapoptotic) [70]. ‡

Activate TLR7 [75]. ⁑

Downregulated in glioma cell lines, inhibits proliferation and migration, increases apoptosis [76]. ∞ *

Protection against oxidative damage [77]. ∞ ‡

Tumor suppressor miRNA, targets the aromatase gene (CYP19A1) [78]. ∞


SCI, TBI, Il-1β and TNF-α stimulation

Upregulated in ADEV after Il-1β and TNF-α stimulation in primary rat astrocytes [63]. Upregulated in rat tissue after SCI [79]. Downregulated in human serum and mouse model after TBI [80].

Biomarker, dysregulated in ALS serum, showed lower expression in slower progressing ALS [81]. Key implication in subacute stage of SCI [82]. •

Reduce dendritic complexity and growth, spike rates and burst activity after inflammatory stimulus. Downregulates NTRK3 and Bcl2 [63]. Stimulates apoptosis and inflammatory proteins, Targets Apelin-13 inactivating ERK1/2 pathway [79]. ‡

Increases apoptosis, causes inflammation [83]. ⁑

Downregulated in glioma cell lines, targets TLN1 to increase glioma viability, proliferation, migration and invasion after TIIA [84]. ∞ *

Decreases fracture healing. Negatively regulates Bcl-2 and Cyclin-D1, therefore suppressing osteogenic differentiation, and osteoblast proliferation and survival. Inhibited proliferation promoting cell-cycle arrest and apoptosis [80]. π



Downregulated in ADEV after HIBD in rat [68].

Potential regulator of robust differentially expressed genes causing downregulation of GABAergic synapse and signaling pathways in AD [85]. It also counter IRE1a pathway downregulating TXNIP, NL3P inflammasome activation and Il-1β production [86]. Reduces inflammation related proteins after HIBD with lower production of TNF-α and IL-1β [68]. •

Reduces neuronal death and apoptosis after HIBD [68]. ‡

Promotes proliferation of activated astrocytes after SCI [87]. *

Upregulated in AD, in microglia adjacent to Aβ deposits. Targets autophagy receptor NBR1 inhibiting clearance of Aβ [88][89]. ⁑

Targets APP expression [90], BNIP2, SOD, GSH-Px and CAT expression, and reduces apoptosis and inflammation after OGD [68]. ∞ ⁑

Expression increased after myocardial infarction. Inhibition associated with cardiomyocyte survival through STAT3 targeting [91]. γ

Promotes osteoclastogenesis via targeting PTEN [92]. Promotes osteogenic differentiation and ossification, and cytokines such as VEGF [93]. π

Upregulated in various cancers, Reduced proliferation in GIST tissue samples, targets KIT expression [94]. ∞



Identified in ADEV from ALS mSOD1 mouse model with neurodegeneration stage not specified, upregulated [69]. Overexpressed in hippocampus after ischemia in rat [95].

Reduced expression in axons in alcoholism and depression [96]. Suppresses OGD induced apoptosis, and Faslg pro-apoptotic factor levels. Upregulated in neurons of the IBZ [97]. ‡

Upregulation in mSOD1 ADEV mouse model is stopped after miR-146a induction [69]. After ISCI injury, stimulates polarization of reactive neurotrophic neuroprotective astrocytes [98]. *

Repress FasL in microglia o inhibit neurotoxic hypoxia activated microglia [99]. ⁑

Diminish apoptosis modulating tumor suppressor PDC4I3K/AKT/GSK-3β, including apoptosis triggered by neurotoxic Aβ1–42 in SH-SY5Y [100]. PTEN independent oncogene [96]. ∞ ‡

Upregulates VEGF promoting angiogenesis in transformed and non-transformed non CNS tumoral cell lines [101]. ∞



Upregulated in ADEV under IPC in rat [65].

Differentially upregulated in MS, associated with non-progressive forms of the disease [9]. Downregulated in ALS [102]. Elevated in PD 6- hydroxydopamine induced rat models [103]. •

Involved in diabetic retinopathy with possible biomarker applications, regulates angiogenesis [104]. ⸰

Targets SIRT1 inhibiting autophagy of the mitochondria [103].

Suppresses lysosomal biogenesis and autophagy by inhibiting TFEB targets pre-transcriptionally [105]. ∞



Downregulated in ADEV after HIBD in rat [68].

Involved in the maintenance of myelin fine tuning SLC45A3 and CLDN-11 expression [106]. ˟

Downregulated in glioma, targeted ABCC4 and EZH2, it reduces proliferation and migration [107]. ∞ *

Upregulated in some cancer tissues, reduces apoptosis and promotes proliferation and migration targeting OTUD3 and promoting MYC [108][109]. ∞


Ischemia, OSA, ASCI

Upregulated in ADEV under IPC in rat [65].

Reduces inflammation after ischemic stroke. Downregulated in OSA, apnea, hypopnea [110]. Downregulated after ASCI, promotes functional recovery after ASCI [111]. •

Diminishes apoptosis, cell death, mitochondrial dysfunction and favors neurite growth [65][111], including IHR induced apoptosis. Decreases ROS production, MAOA hyperactivity and PTEN expression. Promotes phosphorylation of AKT, and GAP43 and NF-200 expression

[110][111]. ‡

Inhibits IHR-induced NF-κB1, PTGS1, TNF-α, and TGF-β expression [110]. +

Downregulated under hypoxia conditions in PASMCs, reverse proliferation and cell cycle induced under hypoxia conditions [112]. ζ

Inhibits IHR-induced apoptosis and CXCL5 and ADRB1 expression [110]. ∞, α

Regulate proliferation, apoptosis, differentiation, and metastasis[112]. ∞


Il-1β stimulation

Upregulated in ADEV under Il-1β and ATP induction in primary rat astrocytes [63].

Downregulated in autosomal recessive NDD SMA [113][114].. ⸸

Induces apoptosis in retinal ganglion cells exposed to H2O2 [115]. ‡

Activates TLR8 receptors post-translationally causing indirect neuronal microenvironment dysregulation, activates cytokine and chemokine release [116] Downregulates in activated microglia, ameliorates motor function loss after SCI by targeting TLR4 and NF-κB [117]. ⁑

Activates cytokine and chemokine release in macrophages [116]. α

Downregulated in hypoxia induced proliferation of PASMCs, suppress mTOR expression leading to inhibition of proliferation [118]. ζ

Overexpressed in EVs from CRC cells mutant KRAS expressing [119] ∞ ο


TNF-α stimulation

Upregulated in ADEV after TNF-α stimulation in primary rat astrocytes [63].

Involved in AD, targets BACE1, CDK5, ADAM1, increases neuronal differentiation [120]. •

Higher expression correlates with lower overall patient survival in high grade gliomas [121]

Alter key aggressiveness characteristics of prostate cancer cells such as proliferation, modulates lipid metabolism, adjacent non-tumoral tissue shows downregulation. Its expression in cancer correlates with levels in plasma [122]. ∞


Morphine-mediated neuroinflammatory microenvironment

Upregulated in ADEV under morphine stimulated conditions in mouse [58].

Activates astrocytes induced by Tat in HAND [123]. *

Internalizes mir-138 charged ADEV. Activation of microglia through direct activation of the TLR7-NF-kB axis [58].⁑

Promotes early differentiation of oligodendrocytes [124]. ˟

Inhibits adipocyte differentiation reducing EZH2 expression [125]. μ


Early asymptomatic mSOD1 ALS model, ethanol activated neuroinflammation

Upregulated in ADEV after ethanol induction in mouse astrocytes [66], Identified in ADEV from ALS mSOD1 mouse model with neurodegeneration stage not specified, downregulated [69].

Involvement in pathogenesis of MS, AD, prion disease, neurotropic virus and metal sulfate induced toxicity [126] and neuroprotective in specific contexts in ALS and stroke [69][127]. •

Upregulated after stroke in NPC. Increases myelinization protein expression and differentiation towards oligodendrocyte lineage [127]. ⸸ ˟

Increases inflammation and its own expression in cortical neurons [66]. ‡

Attenuates miR-21 and miR-155 expression in ALS mSOD1 mouse model, decreases astrocyte reactivity and decreases proinflammatory miRNA associated exosomal cargo production [69]. Downregulated in ALS [128]. *

Downregulated by infection (RCV virus), it diminish TRAF-6 expression, JNK activation and lung inflammatory infiltration, reduces L-1β, IL -6 and TNF-α production [129]. e



Neuroinflammation, proinflammatory cytokines

Identified in ADEV from ALS mSOD1 mouse model with neurodegeneration stage not specified, upregulated [69]. Downregulated in spinal cord of mice with EAE [130].

Globally upregulated in AD, related with inflammation targets CFH [120][126].. Upregulated in EAE MS mouse model [131], it expression is very high in MS lesions, favors proinflammatory conditions and negatively regulates BBB [126][130]. •

Downregulated in ADEV in ALS mSOD1 mouse model by miR-146a induction [69] *

Upregulated by proinflammatory cytokines [69]. Downregulates fatty acid metabolism associated genes [130]. +

Increases macrophage migration, mediates activation of mononuclear phagocytes, [132] α

Constitutively highly expressed [126], promotes differentiation of TH17 cells and activation of T-cells and dendritic cells [130]. δ

ROS diminish miR-155-5p expression in tumor exosomes leading to immunosuppressive tumor growth [132]. ∞


SCI, HIBD, LPS Ethanol induced neuro-inflammation

Downregulated in ADEV after HIBD in rat [68], upregulated in ADEV after ethanol induction in mouse astrocytes [66] Downregulated in SCI of mice [133].

Anti-inflammatory miR [133]. After ischaemia exacerbates BBB dysfunction [134]. •

Enriched in neurons. Increased dendrite tree complexity, axon and neurite outgrowth, favoring expression of neurofilament-M and neurofilament-L, and AKT phosphorylation [135]. Improves SCI reducing apoptosis [133]. ⸸ ‡

Increases in ethanol-treated wild type astrocytes in a TLR4-dependent response [66]. *

Inflammatory suppressor (downregulates TNF-α, IL-6, IL-1β), apoptosis reduction by caspase-3 downregulation. Decreases expression after LPS [133]. ∞ ⁑

Targeted MTSS1 tumor suppressor transcript to inhibit proliferation and migration in glioma [136]. ∞

Inhibited apoptosis regulating PDCD4 and PACS2, under non-ischemic heart failure [137]. γ

Downregulated after Ischemia Reperfusion (I/R). It reduces autophagy stimulating mTOR and targeting Deptor, thus reducing lesion area after I/R [138]. ο

Biomarker in prostate cancer [139]. ∞


Ethanol induced neuro-inflammation

Upregulated in ADEV after ethanol induction in mouse astrocytes [66], downregulated in ADEV after HIBD in rat [68].

Targets APP gene downregulating amyloid beta (Aβ), however Aβ42 inhibits its expression (possibly halts AD progression) [140]. •

Increases in ethanol treated wild type astrocytes in a TLR4-dependent response [66]. *

Upregulated by Aβ, its transfection reduces Aβ secretion in conditioned media, relieve memory impairments and downregulates targets such as IRS-1pSer potentially diminishing insulin resistance [141]. ‡

Under glucotoxicity increases apoptosis of human retinal pigment epithelial cells [142]. ε



Upregulated after TBI induction in mouse [67].

Improve neurological deficits associated with TBI, exhibiting a neuroprotective role regulating inflammatory signals [67]. Targets A20 (TNFAIP3) and targeted by HOTAIRM1 a miR-sponge associated with neuronal apoptosis [143][144]. •

Released by activated astrocytes [67]. *

Decreases ERK and NF-κB p65 phosphorylation inhibiting LPS induced M1 phenotype and inflammatory signaling, promotes microglia M2 polarization after TBI [67]. ⁑

Proapoptotic inhibitor of cell growth, downregulated in glioblastoma [145]. ∞

Target cells: ‡-Neurons, *-Astrocytes, ⁑-Microglia, ˟-Oligodendrocyte/OPCs, ⸸-Neural Progenitor/Neural Stem cell, +-Endotelial cells, •-CNS non-identified tissue, α-Monocyte/Macrophage, γ-Cardiomyocytes, δ-Limphocytes, ε-Epithelial cells, ζ- Smooth Muscle cells, μ-Preadipocyte/Adipocyte, ο-Enterocytes/Intestinal mucosa epitelial, π-Osteoblasts/Osteogenic precursor, ∞-Cancer, ⸰-non-specified peripheral origin.

This entry is adapted from the peer-reviewed paper 10.3390/life12111720


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