Anti-Myofibroblasts antibody [PR 2D3]

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Myofibroblasts also known as alpha-SMA-positive fibroblasts play a mechanical role in wound healing and tissue repair. These cells express the alpha-smooth muscle actin (α-SMA) protein which has a molecular mass of about 42 kDa. Myofibroblasts are highly contractile and can generate force similar to smooth muscle cells. They appear in various tissues where they contribute to the extracellular matrix (ECM) remodeling by producing collagen and fibronectin aiding in tissue repair and fibrosis.

Biological function summary

Myofibroblasts are active players in tissue remodeling processes. They are not part of a large complex but interact closely with other ECM components. These cells possess a high proliferative capacity and under certain conditions can differentiate from fibroblasts epithelial cells or pericytes. The differentiation involves a dynamic process controlled by transforming growth factor-beta 1 (TGF-β1) which induces stress fiber formation and ECM deposition. Myofibroblasts secrete cytokines and growth factors that modulate inflammation and cellular communication within the tissue.

Pathways

Myofibroblast differentiation and function are closely linked to the TGF-β signaling pathway and the Wnt signaling pathway. TGF-β is an important regulator that promotes the expression of α-SMA and the synthesis of ECM proteins. Important related proteins include fibronectin and collagen types I and III which are influenced by TGF-β signals. In the Wnt signaling pathway myofibroblasts can mediate cross-talk with other cell types affecting pathway components like β-catenin further influencing tissue repair and fibrosis.

Myofibroblasts have been implicated in fibrosis and cancer. In fibrosis excessive activation and accumulation of myofibroblasts lead to abnormal ECM deposition resulting in conditions like hepatic or pulmonary fibrosis. In cancer they contribute to the desmoplastic reaction altering the tumor microenvironment and potentially promoting tumor progression. Myofibroblasts interact with proteins such as matrix metalloproteinases (MMPs) in fibrosis which modify the ECM and in cancer they secrete growth factors that can influence epithelial-to-mesenchymal transition (EMT) linking them to disease progression.