Why cellular stress suppresses adipogenesis in skeletal tissue, but is ineffective in adipose tissue: Control of mesenchymal cell differentiation via integrin binding sites in extracellular matrices

Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA. Electronic address: .
Matrix biology: journal of the International Society for Matrix Biology (Impact Factor: 5.07). 06/2013; 32(7). DOI: 10.1016/j.matbio.2013.06.001
Source: PubMed


This Perspective addresses one of the major puzzles of adipogenesis in adipose tissue, namely its resistance to cellular stress. It introduces a concept of "density" of integrin binding sites in extracellular matrix, proposes a cellular signaling explanation for the observed effects of matrix elasticity and of cell shape on mesenchymal stem cell differentiation, and discusses how specialized integrin binding sites in collagen IV - containing matrices guard two pivotal physiological and evolutionary processes: stress-resistant adipogenesis in adipose tissues and preservation of pluripotency of mesenchymal stem-like cells in their storage niches. Finally, it proposes strategies to suppress adipogenesis in adipose tissues.

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Available from: Bjorn R Olsen, Jan 04, 2014
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    • "While this could be one explanation, there could also be thresholds of MSC-ECM interactions that must be reached before certain effects occur. Indeed, a similar idea was proposed by Volloch and Olsen [36] regarding the effect that the " density " of integrin-binding sites within various matrices has on MSC differentiation. In addition to these quantitative thresholds of interacting ECM, apparently achieved in the OBC matrix studied here, there are likely qualitative characteristics of the OBC matrix, i.e., specific components that are important for the control of the differentiation activities of MSCs. "
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