Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 479, Issue 1, Pages 74-81Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2008.07.029
Keywords
Compound C; Adipogenesis; Mitotic clonal expansion; AMP-activated protein kinase; p21; Protein stability
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Funding
- Korea government (MEST) [R11-2007-107-01001-0]
- National Research Foundation of Korea [과C6A2102, R11-2007-107-01001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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AMP-activated protein kinase (AMPK) activation inhibits adipocyte differentiation. This study investigated the effect Of compound C (CC), a Widely used AMPK inhibitor, oil differentiation of 3T3-L1 preachpocytes. CC treatment blocked hormone-induced preadipocyte differentiation due to inhibition of mitotic clonal expansion, which was accompanied by the failure of degradation of p21, a cyclin-dependent kinase inhibitor. CC increased the level of p21 protein, but not its mRNA, in preadipocytes incubated in a hormone-free medium. Cycloheximide decreased the basal p21 level, which was inhibited by CC treatment, Supporting the stabilization of p21 by CC. Treatment of AICAR OF metformin, AMPK activators, failed to induce p21 or inhibit the ability of CC to increase p21 level. In conclusion, CC inhibits proliferation of preadipocytes as a consequence of an increase in p21 content, which might result from p21 stabilization, and the increase in p21 level by CC might not be associated with AMPK inhibition. (c) 2008 Elsevier Inc. All rights reserved.
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