Matrix control of transforming growth factor-β function

被引:204
作者
Horiguchi, Masahito [1 ]
Ota, Mitsuhiko
Rifkin, Daniel B.
机构
[1] NYU, Sch Med, Dept Cell Biol, New York, NY 10016 USA
关键词
elastic microfibrils; extracellular matrix; integrin; TGF-beta paradox; transforming growth factor-beta; ACTIVATES LATENT TGF-BETA-1; TGF-BETA; EXTRACELLULAR-MATRIX; MEDIATED ACTIVATION; IN-VIVO; BINDING-PROTEINS; LUNG DEVELOPMENT; MOUSE MODEL; LONG FORM; ELASTOGENESIS;
D O I
10.1093/jb/mvs089
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The cytokine transforming growth factor-beta (TGF-beta) has multiple effects in both physiological and pathological conditions. TGF-beta is secreted as part of a tripartite complex from which it must be released in order to bind to its receptor. Sequestration of latent TGF-beta in the extracellular matrix (ECM) is crucial for proper mobilization of the latent cytokine and its activation. However, contrary to expectation, loss-of-function mutations in genes encoding certain matrix proteins that bind TGF-beta yield elevated, rather than decreased, TGF-beta levels, posing a 'TGF-beta paradox.' In this review, we discuss recent findings concerning the relationship of TGF-beta, ECM molecules, and latent TGF-beta activation and propose a model to resolve the 'TGF-beta paradox.'.
引用
收藏
页码:321 / 329
页数:9
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