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Am J Physiol Heart Circ Physiol (September 2, 2005). doi:10.1152/ajpheart.00321.2005
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Submitted on March 31, 2005
Accepted on September 1, 2005

Type VI collagen induces cardiac myofibroblast differentiation: implications for post-infarction remodeling

Jennifer E Naugle1, Erik R Olson1, Xiaojin Zhang1, Sharon E Mase1, Charles F Pilati1, Michael B Maron1, Hans G Folkesson1, Walter I Horne2, Kathleen J Doane3, and J G Meszaros1*

1 Physiology and Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown, OH, USA
2 Comparative Medicine Unit, Northeastern Ohio Universities College of Medicine, Rootstown, OH, USA
3 Anatomy, Northeastern Ohio Universities College of Medicine, Rootstown, OH, USA

* To whom correspondence should be addressed. E-mail: jgmeszar{at}neoucom.edu.

Cardiac fibroblast (CF) proliferation and differentiation into hypersecretory myofibroblasts can lead to excessive extracellular matrix (ECM) production and cardiac fibrosis. In turn, the ECM produced can potentially activate CFs via distinct feedback mechanisms. To assess how specific ECM components influence CF activation, isolated CFs were plated on specific collagen substrates (collagens I, III, VI) prior to carrying out functional assays. The type VI collagen substrate potently induced myofibroblast differentiation, but had little effect on CF proliferation. Conversely, the type I and III collagen substrates did not affect differentiation but caused significant induction of proliferation (type I: 240.7 +/- 10.3% and type III: 271.7 +/- 21.8% of basal). Type I collagen activated ERK 1/2, whereas collagen III did not. Treatment of CFs with angiotensin II, a potent mitogen of CFs, enhanced the growth observed on types I and III collagen, but not on the type VI collagen substrate. Using an in vivo model of myocardial infarction (MI), we measured changes in type VI collagen expression and myofibroblast differentiation following post-MI remodeling. Concurrent elevations in type VI collagen and myofibroblast content were evident in the infarcted myocardium 20 weeks post-MI. Overall, types I and III collagen stimulate CF proliferation, whereas type VI collagen plays a potentially novel role in cardiac remodeling through facilitation of myofibroblast differentiation.




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