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Papers In Press, published online ahead of print January 20, 2005
J. Biol. Chem, 10.1074/jbc.M410515200
Submitted on September 13, 2004
Revised on December 27, 2004
Accepted on January 20, 2005

Role of Kruppel-like factor 15 (KLF15) in transcriptional regulation of adipogenesis

Toshiyuki Mori, Hiroshi Sakaue, Haruhisa Iguchi, Hideyuki Gomi, Yuko Okada, Yasuhiro Takashima, Kyoko Nakamura, Takehiro Nakamura, Toshimasa Yamauchi, Naoto Kubota, Takashi Kadowaki, Yasushi Matsuki, Wataru Ogawa, Ryuji Hiramatsu, and Masato Kasuga

Department of Clinical Molecular Medicine, Kobe University, Graduate School of Medicine, Kobe 650-0017

Corresponding Author: hsakaue{at}med.kobe-u.ac.jp

Krpel-like zinc-finger transcription factors (KLFs) play diverse roles during cell differentiation and development in mammals. We have now shown by microarray analysis that expression of the KLF15 gene is markedly up-regulated during the differentiation of 3T3-L1 preadipocytes into adipocytes. Inhibition of the function of KLF15, either by expression of a dominant negative mutant or by RNA interference, both reduced the expression of peroxisome proliferatoractivated receptor gamma(PPARgamma) and blocked adipogenesis in 3T3-L1 preadipocytes exposed to inducers of adipocyte differentiation. However, the dominant negative mutant of KLF15 did not affect the expression of CCAAT/enhancerbinding protein beta (C/EBPbeta) elicited by inducers of differentiation in 3T3-L1 preadipocytes. In addition, ectopic expression of KLF15 in NIH 3T3 or C2C12 cells triggered both lipid accumulation and the expression of PPARgamma in the presence of inducers of adipocyte differentiation. Ectopic expression of C/EBPbeta, C/EBPdelta or C/EBPalpha in NIH 3T3 cells also elicited the expression of KLF15 in the presence of inducers of adipocyte differentiation. Moreover, KLF15 and C/EBPalpha acted synergistically to increase the activity of the PPARgamma2 gene promoter in 3T3-L1 adipocytes. Our observations thus demonstrate that KLF15 plays an essential role in adipogenesis in 3T3-L1 cells through its regulation of PPARgamma expression.


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