Vascular smooth muscle cells in the aorta play an integral role in regulating vessel wall contractility and matrix deposition in the medial layer. Recent studies show that mutations in genes associated with actomyosin apparatus reduce smooth muscle contractility, increasing susceptibility to thoracic aneurysm development. These mutations are associated with impaired vascular smooth muscle cell function, which may lead to decreased ability of the cell to sense matrix-mediated mechanical stimuli. This study investigates how loss of smooth muscle alpha-actin affects cell adhesion. We tested the hypothesis that a loss of smooth muscle alpha-actin decreases cell adhesion to the matrix. Confocal and total internal reflection fluorescence microscopy were used to quantify actin and focal adhesion fluorescence, respectively, in wild-type and smooth muscle alpha-actin null cells. Our results showed that in absence of smooth muscle alpha-actin, there is a compensatory increase in smooth muscle gamma-actin. Moreover, specific integrin recruitment at cell-matrix adhesions was reduced in alpha-actin null cells. These findings suggest a dysfunctional vascular smooth muscle cell-matrix cross-talk and cellular mechanosensing in alpha-actin null cells.<br/>

Loss of smooth muscle alpha-actin impairs cellular mechanosensing

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.