西亚试剂：WNT signaling is a key regulator of MSC biology

WNT signaling is a key regulator of MSC biology (Christodoulides et al., 2009 and Krishnan et al., 2006). Canonical signaling, the best-studied pathway, which critically relies on LRP5 and LRP6 co-receptors for activation, has been shown to repress adipogenesis and stimulate osteoblastogenesis. Accordingly, patients carrying rare gain-of-function (GoF) LRP5 mutations exhibit high bone mass (HBM) ( Boyden et al., 2002 and Little et al., 2002). Reciprocally, rare loss-of-function (LoF) LRP5 mutations lead to osteoporosis ( Ai et al., 2005 and Gong et al., 2001), which, in a study of 12 affected probands from two families, was coupled with an increased prevalence of T2D (Saarinen et al., 2010). Finally, rare inactivating missense mutations in LRP6 result in autosomal dominant CVD, features of the metabolic syndrome, and osteoporosis ( Mani et al., 2007 and Singh et al., 2013). Prompted by these and the aforementioned GWAS findings (Heid et al., 2010), we sought to determine the role of LRP5 in human WAT biology and fat distribution. Our interest in LRP5 was also stimulated by preliminary analyses showing that it was differentially expressed between SC abdominal and gluteal SVCs. Furthermore, WAT LRP5 mRNA levels correlated with measures of regional adiposity and systemic insulin sensitivity. Herein we demonstrate that LRP5-driven β-catenin signaling regulates adipose progenitor proliferation and differentiation in a dose- and depot-specific manner, thereby modulating human body fat distribution

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