WOUND HEALING: MYOFIBROBLASTS ARE RESPONSIBLE FOR WOUND CONTRACTION
Myofibroblasts have features of both fibroblasts and smooth muscle cells and are relevant to wound healing (Junqueira et al 2003), especially by secondary intention (Robbins Basic Pathology 2006). TGF-beta 1 is an important inducer of myofibroblast differentiation, a cell that is important in the formation of human peritoneal adhesions and pathogenic in pulmonary fibrotic disease (Thomas et al 2007, and Xu et al 2002).
- Initially were described in granulation tissue and nodules of Dupuytren’s disease.
- In 1970, Tremblay described myofibroblasts in the stroma of mammary carcinomas.
- Myofibroblasts possess contractile forces and synthetic properties (Schurch et al 1997).
- Myofibroblasts possess synthetic properties for collagens (1,3,4,5), glycoproteins, proteoglycans (fibronectin, laminin, tenascin).
- Myofibroblasts synthesize collagen (initially type III); and in granulation tissue undergo apoptosis as the wound matures and closes by epithelialization.
- Myofibroblasts express various cytoskeletal phenotypes:
- Type V (vimentin)
- Type VA (vimentin, plus actin)
- Type VAD (plus desmin)
- Type VD (vimentin and desmin)
- Phenotype VAD (myosin heavy chains without desmin).
- Myofibroblasts are relevant to musculoaponeurotic fibromatosis (Dupuytren's, Ledderhouse, Peyronies disease).
- Myofibroblasts are stimulated by TNF, IL1, TGF-beta , PDGF.
- Myofibroblasts are relevant in wound healing and closure.
- These cells potentially arise from mesenchymal cells and play critical functions in granulation tissue/wound closure/scar tissue formation/pathological scarring.
- In normal wound healing, the fibroblastic reaction appears centripetal. Within neoplastic invasion it is centrifugal, that indicates that cancers are wounds that do not heal (Schurch et al 1997).
Illustration of recalcitrant leg ulcer. By advanced biological wound healing technology and advancement of ulcer contraction, chronic ulcers can be healed by shortening closure time.
Topical application of platelet rich plasma, with activated GF, can enhance ECM, improve granulations, and facilitate epithelialization. Biotechnology TC showing stimulation of fibroblasts ex vivo, that are converted to myofibroblasts, thereby speeding up wound and ulcer contraction.
MYOFIBROBLAST ACADEMIC REFERENCES BY BOLANDCELL
- Junqueira LC et al. Basic Histology: Text and Atlas. Lange, New York, 10th edition, 2003: 97.
- Robbins Basic Pathology. Saunders, Elsevier. 8th edition. Edited by Kumar et al 2006; 76.
- Xu X et al. Role of mast cells and myofibroblasts in human peritoneal adhesion formation. Ann Surg 2002: 236; 593-601.
- Thomas PE et al. PGE2 inhibition of TGF-beta 1-induced myofibroblast differentiation. Am J Physiol Lung Cell Mol Physiol, 2007 June 8 (Epub ahead of print).
- Schurch W et al. Myofibroblast. Chapter 7. Histology for Pathologists, Second Edition, Lippincott, Philadelphia, 1997: 129