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Smooth muscle a actin (Acta2) and myofibroblast function during hepatic wound healing.

Authors: Rockey, Don C  Weymouth, Nate  Shi, Zengdun 
Citation: Rockey DC, etal., PLoS One. 2013 Oct 29;8(10):e77166. doi: 10.1371/journal.pone.0077166. eCollection 2013.
Pubmed: (View Article at PubMed) PMID:24204762
DOI: Full-text: DOI:10.1371/journal.pone.0077166

Smooth muscle α actin (Acta2) expression is largely restricted to smooth muscle cells, pericytes and specialized fibroblasts, known as myofibroblasts. Liver injury, associated with cirrhosis, induces transformation of resident hepatic stellate cells into liver specific myofibroblasts, also known as activated cells. Here, we have used in vitro and in vivo wound healing models to explore the functional role of Acta2 in this transformation. Acta2 was abundant in activated cells isolated from injured livers but was undetectable in quiescent cells isolated from normal livers. Both cellular motility and contraction were dramatically increased in injured liver cells, paralleled by an increase in Acta2 expression, when compared with quiescent cells. Inhibition of Acta2 using several different techniques had no effect on cytoplasmic actin isoform expression, but led to reduced cellular motility and contraction. Additionally, Acta2 knockdown was associated with a significant reduction in Erk1/2 phosphorylation compared to control cells. The data indicate that Acta2 is important specifically in myofibroblast cell motility and contraction and raise the possibility that the Acta2 cytoskeleton, beyond its structural importance in the cell, could be important in regulating signaling processes during wound healing in vivo.

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CRRD Object Information
CRRD ID: 12879446
Created: 2017-04-19
Species: All species
Last Modified: 2017-04-19
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.