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MBC in Press, published online ahead of print August 10, 2005
Mol. Biol. Cell 10.1091/mbc.E05-03-0216

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Submitted on March 16, 2005
Revised on July 7, 2005
Accepted on August 2, 2005

YB-1 Coordinates Vascular Smooth Muscle {alpha}-Actin Gene Activation by TGF{beta}1 and Thrombin during Differentiation of Human Pulmonary Myofibroblasts

Aiwen Zhang,* Xiaoying Liu,* John G. Cogan,* Matthew D. Fuerst,* John A. Polikandriotis,*{dagger} Robert J. Kelm Jr.,{ddagger} and Arthur R. Strauch*

*Department of Physiology and Cell Biology, the Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210; {ddagger}Department of Medicine, College of Medicine, University of Vermont, Colchester, VT 05446

Monitoring Editor: Carl-Henrik Heldin

Profibrotic regulatory mechanisms for tissue repair after traumatic injury have developed under strong evolutionary pressure to rapidly stanch blood loss and close open wounds. We have examined the roles played by two profibrotic mediators, TGF{beta}1 and thrombin, in directing expression of the vascular smooth muscle alpha-actin (SM{alpha}A) gene, an important determinant of myofibroblast differentiation and early protein marker for stromal cell response to tissue injury. TGF{beta}1 is a well known transcriptional activator of the SM{alpha}A gene in myofibroblasts (Subramanian et al., Molec. Biol. Cell 15: 4532-43, 2004). In contrast, thrombin independently elevates SM{alpha}A expression in human pulmonary myofibroblasts at the posttranscriptional level. A common feature of SM{alpha}A up-regulation mediated by thrombin and TGF{beta}1 is the involvement of the cold shock domain protein, YB-1, a potent repressor of SM{alpha}A gene transcription in human fibroblasts that also binds mRNA and regulates translational efficiency. YB-1 dissociates from SM{alpha}A enhancer DNA in the presence of TGF{beta}1 or its Smad 2,3,4 coregulatory mediators. Thrombin does not effect SM{alpha}A gene transcription but rather displaces YB-1 from SM{alpha}A exon 3 coding sequences previously shown to be required for mRNA translational silencing. The release of YB-1 from promoter DNA coupled with its ability to bind RNA and shuttle between the nucleus and cytoplasm is suggestive of a regulatory loop for coordinating SM{alpha}A gene output in human pulmonary myofibroblasts at both the transcriptional and translational levels. This loop may help restrict organ-destructive remodeling due to excessive myofibroblast differentiation.

{dagger}Present address: Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University, Atlanta, GA 30322.

Address correspondence to: Arthur R. Strauch (strauch.1{at}osu.edu)




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