2 results match your criteria: "USA Center of Excellence in Bioinformatics and Life Sciences[Affiliation]"

Cadherin-11 is a novel regulator of extracellular matrix synthesis and tissue mechanics.

J Cell Sci

August 2016

Department of Chemical and Biological Engineering, University at Buffalo, State University of New York, Amherst, NY 14260, USA Department of Biomedical Engineering, University at Buffalo, State University of New York, Amherst, NY 14260, USA Center of Excellence in Bioinformatics and Life Sciences, Buffalo, NY 14203, USA

We discovered that Cadherin-11 (CDH11) regulates collagen and elastin synthesis, both affecting the mechanical properties and contractile function of animal tissues. Using a Cdh11-null mouse model, we observed a significant reduction in the mechanical properties [Youngs' modulus and ultimate tensile strength (UTS)] of Cdh11(-/-) as compared to wild-type (WT) mouse tissues, such as the aorta, bladder and skin. The deterioration of mechanical properties (Youngs' modulus and UTS) was accompanied by reduced collagen and elastin content in Cdh11(-/-) mouse tissues as well as in cells in culture.

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Cadherin-11 regulates both mesenchymal stem cell differentiation into smooth muscle cells and the development of contractile function in vivo.

J Cell Sci

June 2014

Bioengineering Laboratory, Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Amherst, NY 14260-4200, USA Department of Biomedical Engineering, University at Buffalo, The State University of New York, Amherst, NY 14260-4200, USA Center of Excellence in Bioinformatics and Life Sciences, Buffalo, NY 14203, USA

Although soluble factors, such as transforming growth factor β1 (TGF-β1), induce mesenchymal stem cell (MSC) differentiation towards the smooth muscle cell (SMC) lineage, the role of adherens junctions in this process is not well understood. In this study, we found that cadherin-11 but not cadherin-2 was necessary for MSC differentiation into SMCs. Cadherin-11 regulated the expression of TGF-β1 and affected SMC differentiation through a pathway that was dependent on TGF-β receptor II (TGFβRII) but independent of SMAD2 or SMAD3.

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