Stable SREBP-1a knockdown decreases the cell proliferation rate in human preadipocyte cells without inducing senescence.

ALVAREZ MS; FERNANDEZ-ALVAREZ A; CUCARELLA C; CASADO M

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 2014

0006-291X

Sterol regulatory element binding proteins (SREBP), encoded by the Srebf1 andSrebf2 genes, are important regulators of genes involved in cholesterol and fattyacid metabolism. Whereas SREBP-2 controls the cholesterol synthesis, SREBP-1proteins (-1a and -1c) function as the central hubs in lipid metabolism. Despite the key function of these transcription factors to promote adipocytedifferentiation, the roles of SREBP-1 proteins during the preadipocyte stateremain unknown. Here, we evaluate the role of SREBP-1 in preadipocyteproliferation using RNA interference technology. Knockdown of the SREBP-1a genedecreased the proliferation rate in human SGBS preadipocyte cell strain withoutinducing senescence. Furthermore, our data identified retinoblastoma bindingprotein 8 and cyclin-dependent kinase inhibitor 3 genes as new potential SREBP-1 targets, in addition to cyclin-dependent kinase inhibitor 1A which had alreadybeen described as a gene regulated by SREBP-1a. These data suggested a new roleof SREBP-1 in adipogenesis via regulation of preadipocyte proliferation.