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Critical substrate stiffness initiates smooth muscle alpha‐actin promoter activity in myofibroblasts

Tissue contraction is a critical event in wound closure. Myofibroblasts are specialized fibroblasts that facilitate this process through expression of smooth muscle (SM) contractile proteins and generation of contractile forces on the surrounding matrix. However, when this differentiated function becomes disregulated, pathological contractures can result in tissue deformation and loss of function. This project aimed to determine the mechanoregulation involved in myofibroblast differentiation. The hypothesis tested was that a critical stiffness will promote expression of SM‐specific cytoskeletal proteins in myofibroblasts. It has been previously demonstrated that SM α‐actin (SMAA) expression is mechanoregulated at the promoter level. In this study regulation of SMAA expression was characterized using rat embryonic fibroblasts and novel silicone‐based substrata of varying stiffness. Initial findings demonstrated that SMAA promoter activity increased with respect to substrate stiffness. The mechanoregulated activation was substantiated by the presence of increased focal adhesion size and stress fiber formation with respect to stiffness as illustrated with immunofluorescence imaging. The long‐term goal of this work is to understand the cellular regulation of wound healing and tissue contracture via the study of myofibroblast differentiation and function. Funded by NIH grant R01 GM60651.