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
Caroline Tyavambiza
 -- 2100 2023-07-13 16:52:37 |
2 format
Jason Zhu
 Meta information modification 2100 2023-07-14 03:46:34 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Tyavambiza, C.; Meyer, M.; Meyer, S. Cellular and Molecular Events of Wound Healing. Encyclopedia. Available online: https://encyclopedia.pub/entry/46776 (accessed on 12 September 2024).
Tyavambiza C, Meyer M, Meyer S. Cellular and Molecular Events of Wound Healing. Encyclopedia. Available at: https://encyclopedia.pub/entry/46776. Accessed September 12, 2024.
Tyavambiza, Caroline, Mervin Meyer, Samantha Meyer. "Cellular and Molecular Events of Wound Healing" Encyclopedia, https://encyclopedia.pub/entry/46776 (accessed September 12, 2024).
Tyavambiza, C., Meyer, M., & Meyer, S. (2023, July 13). Cellular and Molecular Events of Wound Healing. In Encyclopedia. https://encyclopedia.pub/entry/46776
Tyavambiza, Caroline, et al. "Cellular and Molecular Events of Wound Healing." Encyclopedia. Web. 13 July, 2023.
Cellular and Molecular Events of Wound Healing
Edit
This entry is adapted from the peer-reviewed paper 10.3390/bioengineering9110712

Chronic wounds are a silent epidemic threatening the lives of many people worldwide. They are associated with social, health care and economic burdens and can lead to death if left untreated. The treatment of chronic wounds is very challenging as it may not be fully effective and may be associated with various adverse effects. New wound healing agents that are potentially more effective are being discovered continuously to combat these chronic wounds. These agents include silver nanoformulations which can contain nanoparticles or nanocomposites. To be effective, the discovered agents need to have good wound healing properties which will enhance their effectiveness in the different stages of wound healing.

wound healing antimicrobial antioxidant silver nanoformulations

1. Introduction

Wound repair is a complex process that involves the coordinated interaction of various cell types, extracellular matrix molecules (ECM) and soluble mediators such as cytokines, chemokines and growth factors [1]. Wound healing is carefully divided into critical stages that happen simultaneously namely haemostasis, inflammatory, proliferation and remodelling phase [2]. These stages are equally important and failure of any one of them can disrupt the wound healing process and lead to the development of chronic wounds. New wound healing treatments are continually being discovered in a bid to find treatments that are effective in all stages of wound healing. Silver has a long history of use in the treatment of wounds. It has been widely reported to have anti-inflammatory and antimicrobial activities (even against multidrug resistant microorganisms such as methicillin-resistant S. aureus (MRSA) and P. aeruginosa) [3]. The proposed mechanisms of antimicrobial action of silver and silver nanoparticles (AgNPs) have been described in literature. Briefly, silver ions can interact with sulphur containing proteins, bind to the cell membrane and cause the disruption of the bacterial cell wall. This will eventually affect the permeability of the membrane causing leakage of metabolites, leading to cell death [4][5]. The silver ions also interfere with the electron transport system leading to increased ROS production, protein synthesis inhibition and denaturation of bacterial DNA thus inhibiting cell replication [6][7]. The anti-inflammatory activity of AgNPs are exerted through decreasing the effects of pro-inflammatory cytokines (IL 6, IL 8, IL 1beta, TNF alpha, MMP 9) [8][9][10][11], increasing the expression of anti-inflammatory cytokines (IL 10) [8] and promoting inflammatory cell death via apoptosis instead of necrosis [12]. Many silver-based compounds including colloidal silver (Silver sulfadiazine (SSD)) and nanosilver (AgNPs, nanocrystalline, nanocomposites) have been used to make wound healing creams, bandages and hydrogels [13]. Although these silver-based formulations have improved the healing of wounds, newer formulations that are potentially more effective are continuously being discovered. Since the wound healing process is divided into different stages, it is important to understand the mechanisms of each stage in-order to promote its effectiveness.

2. Cells Involved in Wound Healing

2.1. Neutrophils

The wound healing process is orchestrated by different cells and signaling molecules. Neutrophils are the first cells to infiltrate the wound site after injury. The infiltration is facilitated by different signaling molecules and chemoattractants such as damage associated molecular patterns (DAMPs) released by necrotic cells, TGF-β, complement molecules (C3a and C5a), hydrogen peroxide (H2O2), chemokines and mediators from platelets [14][15]. CXCL8, one of the most common chemokines released by platelets α-granules, together with CXCL1, and CXCL2 play an important role in initiating inflammatory cell recruitment [16]. DAMPs released from damaged cells are known to be first signals to recruit neutrophils after tissue injury. They can directly activate neutrophils by binding to the specific Pattern Recognition Receptors (PRRs) such as toll-like receptors (TLRs) or indirectly by stimulating other cells to release neutrophil chemoattractants [17][18]. At the wound site, the recruited neutrophils also release some pro-inflammatory mediators such as TNF-α, IL-1β, IL-6 and CXCL8 which will recruit more neutrophils and other immune cells thus further promoting inflammation [19].
The main function of neutrophils is to prevent infections in the inflammatory phase by clearing the wound of any pathogens, foreign particles, and damaged tissue. They achieve this through phagocytosis, generation of an oxidative burst (due to reactive oxygen species (ROS)) and through the release of destructive proteases, antimicrobial proteins (cathepsins, defensins, lactoferrin, lysozyme) and neutrophil extracellular traps [15][20]. Neutrophils can also promote angiogenesis and the proliferation of fibroblasts and keratinocytes by increasing the expression of the cytokines; VEGF, CXCL3, IL-8, IL-1 β and MCP-1 which promote angiogenesis and proliferation [19]. After completing their task, neutrophils need to be eliminated from the wound site. These cells therefore undergo apoptosis and are subsequently phagocytized by macrophages. The elimination of neutrophils marks the transition from the inflammatory to an anti-inflammatory state [19]. Uncontrolled neutrophil migration prolongs the inflammation process leading to excessive generation of ROS and proteases. The toxic proteases and increased ROS levels degrade the ECM and damages cell membranes leading to prolonged wound healing and formation of chronic wounds [20][21].

2.2. Macrophages

Macrophages play a fundamental role in all phases of wound healing. It has been proven that the presence of macrophages promotes wound healing. Hu and colleagues (2017) reported that the increase of macrophages accelerated wound healing in both normal and diabetic mice [22]. Macrophages are initially monocytes which differentiate into macrophages after entering the tissues. These monocytes are activated and recruited to the wound site by chemoattractants (such as MCP-1) and DAMP molecules. Pro-inflammatory macrophages also referred to as M1 macrophages are involved in the inflammatory phase of wound healing while the M2 macrophages or anti-inflammatory macrophages are involved in the later stages in wound repair [23]. M1 macrophages infiltrate the wound site, 24–48 h after injury. These macrophages are highly phagocytic, they clear the wound area by phagocytosing bacteria, debris and apoptotic neutrophils (efferocytosis) [24]. M1 macrophages activates other inflammatory cells by releasing pro-inflammatory cytokines (TNF- alpha, IL-6, and IL- beta), and growth factors (PDGF, VEGF and TGF-β1) [25]. They also release matrix metalloproteinases (MMPs) which digests the ECM, making room for infiltrating inflammatory cells and aiding migration [15]. This exacerbates efferocytosis and the pro-inflammatory state of the wound. Successful efferocytosis marks the resolution of inflammation and promotes the switch of macrophages from a pro-inflammatory to an anti-inflammatory state [26].
M2 macrophages dominate the anti-inflammatory phase of wound healing. They suppress inflammation by upregulating the expression of pro-resolutory cytokines such as IL-4, IL-10, and IL-13 [27]. They also release growth promoting growth factors including arginase 1, an important factor for effective wound repair and MMPs (MMP-12 and MMP-13) which remodel and strengthen the ECM [24]. Anti-inflammatory macrophages promote new vessel formation, angiogenesis, re-epithelialization, and the transition of fibroblasts to myofibroblasts [15][23]. Recent studies suggest that macrophages are also involved in wound resolution, the final phase of wound healing. This involves the release of anti-angiogenic factors, phagocytosis of apoptotic endothelial cells and the maturation of the epithelium [23][28].

2.3. Fibroblasts and Keratinocytes

Fibroblasts which form the major cellular component of the dermis are the key cells in the proliferation phase of wound healing. They are activated by the release of inflammatory signals mainly PDGF and TGF-beta from platelets and macrophages [14][25]. At the wound site, fibroblasts proliferate and synthesize type 1 and III collagen. They also secrete precursors for components of the ECM including hyaluronan, fibronectin, glycosaminoglycans and proteoglycans. Accumulation of the ECM is essential for the repair process as it supports cell migration [2]. Moreover fibroblasts can differentiate into myofibroblasts causing the wound to contract by contracting the wound bed and bringing the wound edges together [14].
Activated fibroblasts secrete paracrine factors such as FGF-2 and KGF which signals adjacent keratinocytes. Keratinocytes respond to these signals by producing PDGF which further stimulates fibroblasts. This kind of interaction between 2 cell types is known as cross talk [29]. Keratinocytes are the predominant cells in the epidermis, their main function in the proliferation phase is re-epithelialization. This is a crucial process which is responsible for restoring an intact epidermis after injury. Epithelialization is a multi-step process involving the proliferation, migration and differentiation of keratinocytes [30][31]. Keratinocytes also stimulate and coordinate the actions of other cell types involved in wound healing. They induce endothelial cell migration and angiogenesis via the secretion of angiogenic growth factors such as VEGF and PDGF [29][32].

3. Role of Cytokines and Growth Factors in Wound Healing

Wound healing is a complex process that involves several cell types and is controlled by various molecules, essentially cytokines and growth factors. The release of these cytokines and growth factors is programmed for each of the different phases of wound healing. Any disruption to this carefully orchestrated process may lead to the formation of non-healing chronic wounds. After injury, the pro-inflammatory cytokines, IL-1β, TNF-α and IL-6 are released to attract inflammatory cells to the wound site [21]. Chemokines such as CXCL8 (IL8), CXCL1, and CXCL2 are also released to help this process of chemotaxis [16]. At the wound site, inflammatory cells mainly macrophages release the growth factors, PDFG and TGF-beta which will recruit fibroblasts, initiating the proliferation phase. Active fibroblasts and macrophages release FGF-2 (bFGF), KGF (FGF-7), EGF, HGF, TGF-α and IGF-1 to stimulate keratinocytes which are essential in epithelization [25][29][33]. Fibroblasts, keratinocytes and macrophages further releases VEGF and PDGF to activate endothelial cells and initiate the process of angiogenesis [25]. As wound healing is a continuous and overlapping process most cytokines and growth factors function in more than 1 phase. There are also other signaling molecules involved in wound healing.

4. Gene Expression in Wound Healing

Wound healing is orchestrated by various genes which code for different signaling molecules (cytokines, chemokines and growth factors) at the different stages of wound healing. The gene expression profile at the site of the wound varies during the different stages of wound healing. The genes are up or down regulated at different stages thus varying the influx and efflux of signaling molecules at the wound site. During the inflammatory phase, the expression of genes which code for pro-inflammatory cytokines, some chemokines and growth factors such as IL-6, TNF-a and IL-8 are upregulated while anti-inflammatory genes such as IL-10 are downregulated [34]. Pro-inflammatory genes coding for TNF activation markers, interferon (IFN) activation markers, leucocytes and macrophage markers were expressed in skin biopsies collected 2 days after wounding in basal cell carcinoma patients [35]. A study by Kubo et al. (2014) showed that the expression levels of IL-1b, IL-6, TNF-a, IFN-c and KC increased 3 h to a day after a skin burn injury in murine models [36]. This is well in the inflammatory phase which is known to take place between 1 h and 3 days after injury [37]. Moniri et al. (2018) reported that treating human dermal fibroblast cells with bacterial nanocellulose/silver (BNC/Ag) nanocomposites increased the expression of TGF-β1 from 4.8- to 11-fold at 6 and 24 h, respectively [38]. TGF-β1 is involved in almost all the processes of wound healing. It prompts the recruitment of inflammatory cells into the injury site, improves the angiogenic properties of endothelial cells, stimulates fibroblast contraction and promotes keratinocyte migration [39][40]. The presence of TGF-β1 is certainly of great importance in the wound healing process. In fact, it was stated that the chronic, nonhealing wounds often show a loss of TGF-β1 signaling [41]. However, prolonged release of this molecule can lead to hypertrophic scar formation. Hypertrophic derived fibroblasts were shown to have prolonged expression of TGF-β1 and TGF-β receptors compared to normal skin fibroblasts. In normal wound healing, the expression of TGF-β receptors decreases during the remodeling phase [41][42][43].
As wound healing proceeds, the expression of genes changes from a pro-inflammatory to that of a repair profile. This gene profile includes genes that promote fibroblasts and keratinocytes proliferation as well as granulation and epithelialization, these include VEGF, PDGF and FGF-2 [34]. Deonarine et al. (2007) showed that even though the proinflammatory genes were increased early (2 days) in the wound, after 4 to 8 days the profile of expressed genes changed to those of repair and angiogenesis. After day 4 and 8, the expression of type IV collagen, procollagen, integrin αv, integrin β5, MMP-2, MMP-9 and progranulin was increased [35]. These genes are involved in proliferation and maturation which occurs between approximately 4 to 21 days of wound healing. Kubo et al. (2014) reported similar results, in which the expression of VEGF, MMP-2, MMP-13 and type I collagen increased after 3 to 14 days in a skin burn injury [37]. Unlike pro-inflammatory cytokines released 3 h after wounding, IL 10 was released after 12 h and lasted up to 7 days post wounding [36]. The remodelling phase, which is the last phase of wound healing, is responsible for the development of new epithelium through restoration of tissue architecture and tissue strength [14]. In this phase, most wound healing genes are downregulated however TGF-β1 and MMPs are upregulated. TGF-β1 stimulates fibroblasts to produce type I and III collagen, while MMPs are responsible for the degradation of collagen. The activity of metalloproteinases is however tightly regulated as it might degrade essential collagen thus causing impaired healing [2][34]. Any disturbances (overexpression, under expression or prolonged expression) in the expression of genes and release of cytokines, chemokines and growth factors in wound healing will disrupt the sequence of healing which may lead to the development of chronic wounds.

References

  1. Dehkordi, A.N.; Babaheydari, F.M.; Chehelgerdi, M.; Raeisi Dehkordi, S. Skin Tissue Engineering: Wound Healing Based on Stem-Cell-Based Therapeutic Strategies. Stem Cell Res. Ther. 2019, 10, 1–20.
  2. Enoch, S.; Leaper, D.J. Basic Science of Wound Healing. Surgery 2008, 26, 31–37.
  3. Rai, M.K.; Deshmukh, S.D.; Ingle, A.P.; Gade, A.K. Silver Nanoparticles: The Powerful Nanoweapon against Multidrug-Resistant Bacteria. J. Appl. Microbiol. 2012, 112, 841–852.
  4. Konop, M.; Damps, T.; Misicka, A.; Rudnicka, L. Certain Aspects of Silver and Silver Nanoparticles in Wound Care: A Minirev. EBSCOhost 2016, 2016, 7614753.
  5. Naik, K.; Kowshik, M. The Silver Lining: Towards the Responsible and Limited Usage of Silver. J. Appl. Microbiol. 2017, 123, 1068–1087.
  6. Yin, I.X.; Zhang, J.; Zhao, I.S.; Mei, M.L.; Li, Q.; Chu, C.H. The Antibacterial Mechanism of Silver Nanoparticles and Its Application in Dentistry. Int. J. Nanomed. 2020, 15, 2555–2562.
  7. Fong, J.; Wood, F. Nanocrystalline Silver Dressings in Wound Management: A Review. Int. J. Nanomed. 2006, 1, 441–449.
  8. Tian, J.; Wong, K.K.Y.; Ho, C.; Lok, C.; Yu, W.; Che, C.; Chiu, J.; Tam, P.K.H. Topical Delivery of Silver Nanoparticles Promotes Wound Healing. ChemMedChem 2007, 2, 129–136.
  9. Wong, K.K.Y.; Cheung, S.O.F.; Huang, L.; Niu, J.; Tao, C.; Ho, C.-M.; Che, C.-M.; Tam, P.K.H. Further Evidence of the Anti-Inflammatory Effects of Silver. ChemMedChem 2009, 4, 1129–1135.
  10. Nadworny, P.L.; Wang, J.; Tredget, E.E.; Burrell, R.E. Anti-Inflammatory Activity of Nanocrystalline Silver in a Porcine Contact Dermatitis Model. Nanomedicine 2008, 4, 241–251.
  11. Tyavambiza, C.; Elbagory, A.M.; Madiehe, A.M.; Meyer, M.; Meyer, S.; Elaissari, A. The Antimicrobial and Anti-Inflammatory Effects of Silver Nanoparticles Synthesised from Cotyledon Orbiculata Aqueous Extract. Nanomaterials 2021, 11, 1343.
  12. Wright, J.B.; Lam, K.A.N.; Buret, A.G.; Olson, M.E.; Burrell, R.E. Early Healing Events in a Porcine Model of Contaminated Wounds: Effects of Nanocrystalline Silver on Matrix Metalloproteinases, Cell Apoptosis, and Healing. Wound Repair Regen. 2002, 10, 141–151.
  13. Nqakala, Z.B.; Sibuyi, N.R.S.; Fadaka, A.O.; Meyer, M.; Onani, M.O.; Madiehe, A.M. Advances in Nanotechnology towards Development of Silver Nanoparticle-Based Wound-Healing Agents. Int. J. Mol. Sci. 2021, 22, 11272.
  14. Velnar, T.; Bailey, T.; Smrkolj, V. The Wound Healing Process: An Overview of the Cellular and Molecular Mechanisms. J. Int. Med. Res. 2009, 37, 1528–1542.
  15. Rodrigues, M.; Kosaric, N.; Bonham, C.A.; Gurtner, G.C. Wound Healing: A Cellular Perspective. Physiol. Rev. 2018, 99, 665–706.
  16. Ridiandries, A.; Tan, J.T.M.; Bursill, C.A. The Role of Chemokines in Wound Healing. Int. J. Mol. Sci. 2018, 19, 3217.
  17. Pittman, K.; Kubes, P. Damage-Associated Molecular Patterns Control Neutrophil Recruitment. J. Innate Immun. 2013, 5, 315–323.
  18. De Oliveira, S.; Rosowski, E.E.; Huttenlocher, A. Neutrophil Migration in Infection and Wound Repair: Going Forward in Reverse. Nat. Rev. Immunol. 2016, 16, 378–391.
  19. Ellis, S.; Lin, E.J.; Tartar, D. Immunology of Wound Healing. Curr. Dermatol. Rep. 2018, 7, 350–358.
  20. Serra, M.B.; Barroso, W.A.; da Silva, N.N.; Silva, S.D.N.; Borges, A.C.R.; Abreu, I.C.; da Rocha Borges, M.O. From Inflammation to Current and Alternative Therapies Involved in Wound Healing. Int. J. Inflamm. 2017, 2017, 3406215.
  21. Beserra, F.P.; Gushiken, L.F.S.; Hussni, M.F.; Pellizzon, C.H. Regulatory Mechanisms and Chemical Signaling of Mediators Involved in the Inflammatory Phase of Cutaneous Wound Healing. In Wound Healing—Current Perspectives; IntechOpen: London, UK, 2018; ISBN 978-1-78985-538-8.
  22. Hu, M.S.; Walmsley, G.G.; Barnes, L.A.; Weiskopf, K.; Rennert, R.C.; Duscher, D.; Januszyk, M.; Maan, Z.N.; Hong, W.X.; Cheung, A.T.M.; et al. Delivery of Monocyte Lineage Cells in a Biomimetic Scaffold Enhances Tissue Repair. JCI Insight 2017, 2, e96260.
  23. Dipietro, L.A.; Wilgus, T.A.; Koh, T.J. Macrophages in Healing Wounds: Paradoxes and Paradigms. Int. J. Mol. Sci. 2021, 22, 950.
  24. Krzyszczyk, P.; Schloss, R.; Palmer, A.; Berthiaume, F. The Role of Macrophages in Acute and Chronic Wound Healing and Interventions to Promote Pro-Wound Healing Phenotypes. Front. Physiol. 2018, 9, 419.
  25. Yussof, S.J.M.; Omar, E.; Pai, D.R.; Sood, S. Cellular Events and Biomarkers of Wound Healing. Indian J. Plast. Surg. 2012, 45, 220.
  26. Khanna, S.; Biswas, S.; Shang, Y.; Collard, E.; Azad, A.; Kauh, C.; Bhasker, V.; Gordillo, G.M.; Sen, C.K.; Roy, S. Macrophage Dysfunction Impairs Resolution of Inflammation in the Wounds of Diabetic Mice. PLoS ONE 2010, 5, e9539.
  27. Wilkinson, H.N.; Hardman, M.J. Wound Healing: Cellular Mechanisms and Pathological Outcomes. Open Biol. 2020, 10, 1–14.
  28. Michaeli, S.; Dakwar, V.; Weidenfeld, K.; Granski, O.; Gilon, O.; Schif-Zuck, S.; Mamchur, A.; Shams, I.; Barkan, D. Soluble Mediators Produced by Pro-Resolving Macrophages Inhibit Angiogenesis. Front. Immunol. 2018, 9, 1–12.
  29. Wojtowicz, A.M.; Oliveira, S.; Carlson, M.W.; Zawadzka, A.; Rousseau, C.F.; Baksh, D. The Importance of Both Fibroblasts and Keratinocytes in a Bilayered Living Cellular Construct Used in Wound Healing. Wound Repair Regen. 2014, 22, 246.
  30. Piipponen, M.; Li, D.; Landén, N.X. The Immune Functions of Keratinocytes in Skin Wound Healing. Int. J. Mol. Sci. 2020, 21, 8790.
  31. Mi, B.; Liu, J.; Liu, G.; Zhou, W.; Liu, Y.; Hu, L.; Xiong, L.; Ye, S.; Wu, Y. Icariin Promotes Wound Healing by Enhancing the Migration and Proliferation of Keratinocytes via the AKT and ERK Signaling Pathway. Int. J. Mol. Med. 2018, 42, 831–838.
  32. Barrientos, S.; Stojadinovic, O.; Golinko, M.S.; Brem, H.; Tomic-Canic, M. PERSPECTIVE ARTICLE: Growth Factors and Cytokines in Wound Healing. Wound Repair Regen. 2008, 16, 585–601.
  33. Seeger, M.A.; Paller, A.S. The Roles of Growth Factors in Keratinocyte Migration. Adv. Wound Care 2015, 4, 213.
  34. Diller, R.B.; Tabor, A.J. The Role of the Extracellular Matrix (ECM) in Wound Healing: A Review. Biomimetics 2022, 7, 87.
  35. Deonarine, K.; Panelli, M.C.; Stashower, M.E.; Jin, P.; Smith, K.; Slade, H.B.; Norwood, C.; Wang, E.; Marincola, F.M.; Stroncek, D.F. Gene Expression Profiling of Cutaneous Wound Healing. J. Transl. Med. 2007, 5, 1–11.
  36. Kubo, H.; Hayashi, T.; Ago, K.; Ago, M.; Kanekura, T.; Ogata, M. Temporal Expression of Wound Healing-Related Genes in Skin Burn Injury. Leg. Med. 2014, 16, 8–13.
  37. Lande’n, N.X.; Li, D.; Stahle, M. Transition from Inflammation to Proliferation: A Critical Step during Wound Healing. Cell. Mol. Life Sci. 2016, 73, 3861–3885.
  38. Moniri, M.; Moghaddam, A.B.; Azizi, S.; Rahim, R.A.; Zuhainis, S.W.; Navaderi, M.; Mohamad, R. In Vitro Molecular Study of Wound Healing Using Biosynthesized Bacteria Nanocellulose/ Silver Nanocomposite Assisted by Bioinformatics Databases. Int. J. Nanomed. 2018, 13, 5097–5112.
  39. Pakyari, M.; Farrokhi, A.; Maharlooei, M.K.; Ghahary, A. Critical Role of Transforming Growth Factor Beta in Different Phases of Wound Healing. Adv. Wound Care 2013, 2, 215.
  40. Evrard, S.M.; Daudigier, C.; Mauge, L.; Israël-Biet, D.; Guerin, C.L.; Bieche, I.; Kovacic, J.C.; Fischer, A.M.; Gaussem, P.; Smadja, D.M. The Profibrotic Cytokine Transforming Growth Factor-Β1 Increases Endothelial Progenitor Cell Angiogenic Properties. J. Thromb. Haemost. 2012, 10, 670–679.
  41. Penn, J.W.; Grobbelaar, A.O.; Rolfe, K.J. The Role of the TGF-β Family in Wound Healing, Burns and Scarring: A Review. Int. J. Burn. Trauma 2012, 2, 18–28.
  42. Wang, R.; Ghahary, A.; Shen, Q.; Scott, P.G.; Roy, K.; Tredget, E.E. Hypertrophic Scar Tissues and Fibroblasts Produce More Transforming Growth Factor-Β1 MRNA and Protein than Normal Skin and Cells. Wound Repair Regen. 2000, 8, 128–137.
  43. Schmid, P.; Itin, P.; Cherry, G.; Bi, C.; Cox, D.A. Enhanced Expression of Transforming Growth Factor-Beta Type I and Type II Receptors in Wound Granulation Tissue and Hypertrophic Scar. Am. J. Pathol. 1998, 152, 485.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Biotechnology & Applied Microbiology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Caroline Tyavambiza
,
Mervin Meyer
,
Samantha Meyer
View Times: 301
Revisions: 2 times (View History)
Update Date: 14 Jul 2023
Table of Contents
    1000/1000
    Hot Most Recent
    ScholarVision Creations
    Feedback