Fibroblast cells play a key role in producing and maintaining connective tissue throughout the body. The ability of these cells to differentiate into a more active myofibroblastic phenotype is important during development and wound healing, but prolonged myofibroblast activation can lead to overproduction of extracellular matrix proteins and stiffening of the surrounding tissue. This stiffening can cause heightened differentiation of neighboring fibroblast through force transduction pathways and can lead to detrimental fibrotic pathologies in many organ systems. Atherosclerosis, interstitial lung disease, cirrhosis and heart valve disease are fibrotic diseases that cause significant cost and mortality in our society. Understanding the processes by which cells sense and respond to substrate stiffness is crucial to the treatment of connective tissue diseases. One primary indicator of the myofibroblastic phenotype is the production of α smooth muscle actin (αSMA) bundles called stress fibers which help transmit stress inside the cell and increases the contractility of the cells and their surrounding tissue .
- Bioengineering Division
Integrin-Focal Adhesion Coupling and Substrate Stiffness Affect Smooth Muscle Alpha Actin Expression in Fibroblasts
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Schroer, AK, & Merryman, WD. "Integrin-Focal Adhesion Coupling and Substrate Stiffness Affect Smooth Muscle Alpha Actin Expression in Fibroblasts." Proceedings of the ASME 2012 Summer Bioengineering Conference. ASME 2012 Summer Bioengineering Conference, Parts A and B. Fajardo, Puerto Rico, USA. June 20–23, 2012. pp. 331-332. ASME. https://doi.org/10.1115/SBC2012-80887
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