Myofibroblasts, differentiation

Olson, E.R., Naugle, J.E., Zhang, X., Bomser, J.A., and Meszaros, J.G. 2005. Inhibition of cardiac fibroblast proliferation and myofibroblast differentiation by resveratrol. Am. J. Physiol. 288 H1131-H1138. 

Dugina, V., Fontao, L., Chaponnier, C., Vasiliev, J., and Gabbiani, G. 2001. Focal adhesion features during myofibroblastic differentiation are controlled by intracellular and extracellular factors. J. Cell Sci. 114 3285-3296. 

Masur, S.K., Dewal, H.S., Dinh, T.T., Erenburg, I., and Petridou, S. 1996. Myofibroblasts differentiate from fibroblasts when plated at low density. Proc. Natl. Acad. Sci. USA 93 4219 1223. 

Antl-muscle-specific actin (clone HHF-35) (M) Enzo 1 8000 MWER Recognition of smooth muscle and striated muscle tumors as well as myofibroblastic differentiation... 

Fukunaga M, Ushigome S, Ishikawa E. Ossifying subcutaneous tumor with myofibroblastic differentiation A variant of ossifying fibromyxoid tumor of soft parts Pathol Int. 1994 44 727-734. 

In general, tumors showing pure fibroblastic or myofibroblastic differentiation are uncommon. Only three cutaneous neoplastic proliferations fall into that... 

O Connell JX, Trotter MJ. Fibrosarcomatous dermatofibrosarcoma protuberans with myofibroblastic differentiation a histologically distinctive variant. Mod Pathol. 1996 9 273-278. 

The desmoplastic stroma associated with DAs expresses a variety of inflammatory and stromal markers. The inflammatory cells are mostly T cells (CD3 positive). Scattered B cells (CD20 positive) and macrophages (MAC387 and KPl positive) are also usually present. The spindle cells express alpha-smooth muscle actin, smooth muscle myosin heavy chain, and collagen IV, markers of myofibroblastic differentiation.They are also reported to be positive for heat shock protein 47 and hbronectin, as well as for proteins associated with tissue remolding such as urokinase-type plasminogen... 

Tseng SC, Li DQ, Ma X. Suppression of transforming growth factor-beta isoforms, TGF-beta receptor type II, and myofibroblast differentiation in cultured human corneal and hmbal fibroblasts by amniotic membrane matrix. J Cell Physiol 1999 179 325-35. 

Dahanyaka T, Salibi R, Honnons S, Jones C, Isem NG, Hu JZ, Nathan SD, Grant G, Phipps RP, Sime PJ (2012) Lactic acid is elevated in idiopathic pulmonary fibrosis and induces myofibroblast differentiation via pH-dependent activation of transforming growth factor. Am J Respir Crit Care Med 186(8) 740-751... 

Nonactivating In addition to white blood cell interactions, new PUs should prevent fibroblast to myofibroblast differentiation to [57]... 

Fig. 14.1. The Thl/Th2 balance is central to the regulation of normal wound repair. Tissue injury results in the initiation of an inflammatory response, mediated by a variety of cells and their by-products. Immune cells are recruited and cross-regulate the Thl/ Th2 balance that occurs in response to the cytokine environment. This balance is in turn cross-regulated by the chemokine/chemokine-receptor expression profile, which functions to amplify the inflammatory process. Cells residing in the injured tissue release profibrotic mediators, which promote fibroblast activation, proliferation, and differentiation to the myofibroblast phenotype. Myofibroblasts produce collagen to repair damaged tissue, which is an event that is favored by the inhibition of MMP activity. The Thl/Th2 balance is central to whether a normal or aberrant wound-repair process is established A Thl environment promotes normal tissue resolution (fibrinolysis), whereas a Th2 environment maintains the progression of fibrotic disease (excessive collagen deposition).

Rotating culture vessels such as simulated microgravity systems are primarily used to study 3-D tumor growth and differentiation. However, mixed cell populations combined with matrix proteins can be used to generate a complex microenvironment in which cell-cell interactions and invasion can be measured (95). A similar system has also been described for the coculture of endothelial cells, myofibroblasts, and tumor cell clusters embedded in Matrigel . Differential labeling of the cell populations enables their invasion and the effects of inhibitors to be measured (96). 

The obvious differential expression of miR-205 and sm-a-actin is noteworthy. MiR-205 is likely not associated with smooth muscle differentiation in general since no expression is seen in the VSMC and myofibroblasts. MiR-205 is more likely related to the basal cell characteristics also seen in skin (20). The specific targets and role of miR-205 in differentiation of basal cells are not known (45). The differential expression of miR-21 and sm-a-actin is also interesting but is not as drastic as for miR-205. In addition to myofibroblasts, both smooth muscle cells in colon (46) and myoepithelial cells in breast (44) have been found to express miR-21. 

Evans, R.A., Tian, Y.C., Steadman, R., and Phillips, A.O. 2003. TGF-betal-mediated fibroblast-myofibroblast terminal differentiation—the role of smad proteins. Exp. Cell Res. 282 90-100. 

During the healing process, hybrid cells, known as myofibroblasts, appear in the dermis. They have the morphological characteristics of both fibroblasts and smooth muscle cells. They are responsible for tissue contraction-retraction during healing. Their cytoplasm contains networks of myofilaments that are in contact with specialized zones of the plasma membrane and can interact with the adjacent cells or connective tissue. These myofibroblasts appear to be differentiated fibroblasts that have acquired the properties of smooth muscle cells. Controlled stimulation with DMAE, for example, is a good way to achieve a tightening effect on the skin. 

More than 90% of the body s supply of vitamin A is stored in the liver. The hepatic parenchymal cells are involved in its uptake, storage, and metabolism. Retinyl esters are transferred to hepatic fat-storing cells (also called Ito cells or lipocytes) from the parenchymal cells. The capacity of these fat-storing cells may determine when vitamin A toxicosis becomes symptomatic. During the development of hepatic fibrosis (e.g., in alcoholic liver disease), vitamin A stores in Ito cells disappear and the cells differentiate to myofibroblasts. These cells appear to be the ones responsible for the increased collagen synthesis seen in fibrotic and cirrhotic livers. 

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