期刊
JOURNAL OF CELL SCIENCE
卷 127, 期 12, 页码 2627-2638出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.134833
关键词
Mesenchymal stem cells; Cell-cell adhesion; Adherens junctions; Smooth muscle cells; Differentiation; Vascular contractility
类别
资金
- National Heart and Lung Institute of the National Institutes of Health [R01 HL086582]
- New York Stem Cell Science Fund [C024316]
- Directorate For Engineering
- Div Of Chem, Bioeng, Env, & Transp Sys [1403086] Funding Source: National Science Foundation
Although soluble factors, such as transforming growth factor beta 1 (TGF-beta 1), 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-beta 1 and affected SMC differentiation through a pathway that was dependent on TGF-beta receptor II (TGFbRII) but independent of SMAD2 or SMAD3. In addition, cadherin-11 activated the expression of serum response factor (SRF) and SMC proteins through the Rho-associated protein kinase (ROCK) pathway. Engagement of cadherin-11 increased its own expression through SRF, indicative of the presence of an autoregulatory feedback loop that committed MSCs to the SMC fate. Notably, SMC-containing tissues (such as aorta and bladder) from cadherin-11-null (Cdh11(-/-)) mice showed significantly reduced levels of SMC proteins and exhibited diminished contractility compared with controls. This is the first report implicating cadherin-11 in SMC differentiation and contractile function in vitro as well as in vivo.
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