期刊
GROWTH FACTORS
卷 31, 期 6, 页码 185-198出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/08977194.2013.840297
关键词
ADAM 12S; adipogenesis; brown fat; HB-EGF; white fat
资金
- Eunice Kennedy Shriver National Institute of Child Health & Human Development Grant [1R15HD050299-01A2]
Abnormal adipogenesis leads to excessive fat accumulation and several health disorders. Mouse fibroblasts (MLC) transfected with ADAM 12S and HB-EGF promoted lipid accumulation. Addition of KBR-7785, an ADAM 12S inhibitor, to HB-EGF/ADAM 12S expressing cells suppressed adipogenesis. BrdU incorporation was attenuated and enhanced mitotracker staining was observed in HB-EGF/ADAM 12S cells. Quantitative real time RT-PCR resulted in elevated levels of expression of three brown adipose tissue (BAT) genes (PRDM16, PGC-1 alpha, and UCP-1), while expression levels of the three white adipose tissue (WAT) genes (PPAR gamma, C/EBP alpha, and AKT-1) were unaltered in HB-EGF/ADAM 12S cells. Amino- or carboxy-terminal deletions of HB-EGF (HB-EGF(Delta N) and HB-EGF(Delta C)) co-expressed with ADAM 12S stimulated lipid accumulation. Human epidermoid carcinoma cells (A431) also exhibited lipid accumulation by HB-EGF/ADAM 12S co-expression. These studies suggest ADAM 12S and HB-EGF are involved in cellular plasticity resulting in the production of BAT-like cells and offers insight into novel therapeutic approaches for fighting obesity.
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