| First Author | Maquoi E | Year | 2005 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 25 |
| Issue | 5 | Pages | 1002-7 |
| PubMed ID | 15731491 | Mgi Jnum | J:110045 |
| Mgi Id | MGI:3630365 | Doi | 10.1161/01.ATV.0000160611.68791.c6 |
| Citation | Maquoi E, et al. (2005) Role of Gas-6 in adipogenesis and nutritionally induced adipose tissue development in mice. Arterioscler Thromb Vasc Biol 25(5):1002-7 |
| abstractText | OBJECTIVE: A potential role of growth arrest-specific gene 6 (Gas-6) in energy storage in adipose tissue was investigated in murine models of obesity. Gas-6 is a ligand for the Axl, C-Mer, and Sky family of tyrosine kinase receptors. METHODS AND RESULTS: Whereas Gas-6, C-Mer, and Sky were expressed in mature murine adipocytes, the expression of Axl was restricted to the stromal-vascular fraction, which includes pre-adipocytes. During the in vitro conversion of adipogenic 3T3-F442A cells into mature adipocytes, the expression of Gas-6 increased in undifferentiated confluent pre-adipocytes during a transient phase of growth arrest. On treatment of these cells with an adipogenic medium, Gas-6 expression decreased sharply, coinciding with expression of early adipocytes markers. This modulation was not observed in the nonadipogenic 3T3-C2 cells. The Gas-6 mRNA level was transiently downregulated during nutritionally induced expansion of adipose tissues in vivo. When kept on a standard diet, no significant difference in either total body weight or weight of gonadal or subcutaneous fat pads was observed between Gas-6 deficient and wild-type mice. On exposure to a high-fat diet, however, Gas-6-deficient mice had significantly less fat mass than their wild-type counterparts. CONCLUSIONS: Gas-6 enhances the accumulation of adipose tissue in diet-induced obese mice. |
