Abstract：
:Alpha-smooth muscle actin (SMA), an actin isoform that contributes to cell-generated mechanical tension, is normally restricted to cells of vascular smooth muscle, but SMA can also be expressed in certain non-muscle cells, most notably myofibroblasts. These cells are present in healing wounds, scars, and fibrocontractive lesions where they contribute to fibrosis. In myofibroblasts, cell-generated traction forces associated with SMA contribute to matrix remodeling, but exogenous mechanical forces can also increase SMA expression. Force-induced SMA utilizes a feed-forward amplification loop involving a priori SMA in focal adhesions, the binding of the p38 MAP kinase to SMA filaments, activation of Rho and binding of serum response factor to the CArG-B box of the SMA promoter. Thus, in addition to its importance as a structural protein in tissue remodeling and contraction, SMA may serve as a mechanotransducer, based on its ability to physically link mechanosensory elements and to enhance its own, force-induced expression.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Wang J,Zohar R,McCulloch CAdoi
10.1016/j.yexcr.2005.11.004keywords:
subject
Has Abstractpub_date
2006-02-01 00:00:00pages
205-14issue
3eissn
0014-4827issn
1090-2422pii
S0014-4827(05)00526-4journal_volume
312pub_type
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