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J. Biol. Chem., Vol. 280, Issue 13, 12867-12875, April 1, 2005

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Role of Krüppel-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

From the Department of Clinical Molecular Medicine, Division of Diabetes and Digestive and Kidney Diseases, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan, the ^¶Genomics Science Laboratories, Sumitomo Pharmaceuticals Co. Ltd., Takarazuka 665-0051, Japan, and the ^||Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan

Krüppel-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 proliferator-activated receptor (PPAR) 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/enhancer-binding protein (C/EBP) 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 PPAR in the presence of inducers of adipocyte differentiation. Ectopic expression of C/EBP, C/EBP, or C/EBP in NIH 3T3 cells also elicited the expression of KLF15 in the presence of inducers of adipocyte differentiation. Moreover, KLF15 and C/EBP acted synergistically to increase the activity of the PPAR2 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 PPAR expression.

Received for publication, September 13, 2004 , and in revised form, December 27, 2004.

^* This work was supported by grants from the Yamanouchi Foundation for Research on Metabolic Disorders and the Suzuken Memorial Foundation (to H. S.), the Ministry of Education, Culture, Sports, Science, and Technology of Japan (MEXT) (to H. S., M. K., and W. O.); the 21st Century COE Program "Center of Excellence for Signal Transduction Disease: Diabetes Mellitus as Model" from MEXT (to M. K.), the Cooperative Link of Unique Science and Technology for Economy Revitalization (CLUSTER) from MEXT (to M. K.), and a grant-in-aid for Scientific Research (C) from the Japan Society for the Promotion of Science (to H. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Clinical Molecular Medicine, Division of Diabetes and Digestive and Kidney Diseases, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. Tel.: 81-78-382-5861; Fax: 81-78-382-2080; E-mail: hsakaue{at}med.kobe-u.ac.jp.

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