HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 279, Issue 28, 29761-29766, July 9, 2004

This Article Full Text Full Text (PDF) All Versions of this Article: 279/28/29761    most recent M401303200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yang, R.-Y. Articles by Liu, F.-T. Search for Related Content PubMed PubMed Citation Articles by Yang, R.-Y. Articles by Liu, F.-T. Social Bookmarking                      What's this?

Galectin-12 Is Required for Adipogenic Signaling and Adipocyte Differentiation^*

Ri-Yao Yang, Daniel K. Hsu, Lan Yu, Huan-Yuan Chen, and Fu-Tong Liu

From the Department of Dermatology, University of California Davis School of Medicine, Sacramento, California 95817

Galectin-12 is a member of the galectin family consisting of -galactoside-binding proteins with conserved carbohydrate recognition domains. This protein is preferentially expressed in peripheral blood leukocytes and adipocytes. We previously showed that galectin-12 is induced by cell cycle block at the G₁ phase and causes G₁ arrest when overexpressed (Yang, R.-Y., Hsu, D. K., Yu, L., Ni, J., and Liu, F.-T. (2001) J. Biol. Chem. 276, 20252-20260). Here, we show that the galectin-12 gene is expressed in mouse preadipocytes and is up-regulated when preadipocytes undergo cell cycle arrest, concomitant with acquisition of the competence to undergo differentiation in response to adipogenic hormone stimulation. Following a brief down-regulation 1 day after adipogenic treatment, its expression was once again markedly elevated when cells underwent terminal differentiation. Down-regulation of endogenous galectin-12 expression by RNA interference greatly reduced the expression of the adipogenic transcription factors CCAAT/enhancer-binding protein- and - and peroxisome proliferator-activated receptor- and severely suppressed adipocyte differentiation as a result of defective adipogenic signaling. We conclude that galectin-12 is required for signal transduction that conveys hormone stimulation to the induction of adipogenic factors essential for adipocyte differentiation. The findings suggest that galectin-12 is a major regulator of adipose tissue development.

Received for publication, February 5, 2004 , and in revised form, April 28, 2004.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AF223223.

^* This work was supported by National Institutes of Health Grants RO1 AI20958 and RO1 AI39620. 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 Dermatology, UC Davis School of Medicine, Research III Bldg., Rm. 3100C, 4645 Second Ave., Sacramento, CA 95817. Tel.: 916-734-8504; Fax: 916-734-8386; E-mail: ryyang{at}ucdavis.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S. Zvonic, M. Lefevre, G. Kilroy, Z. E. Floyd, J. P. DeLany, I. Kheterpal, A. Gravois, R. Dow, A. White, X. Wu, et al. Secretome of Primary Cultures of Human Adipose-derived Stem Cells: Modulation of Serpins by Adipogenesis Mol. Cell. Proteomics, January 1, 2007; 6(1): 18 - 28. [Abstract] [Full Text] [PDF]

				M. Baba, J. Wada, J. Eguchi, I. Hashimoto, T. Okada, A. Yasuhara, K. Shikata, Y. S. Kanwar, and H. Makino Galectin-9 Inhibits Glomerular Hypertrophy in db/db Diabetic Mice via Cell-Cycle-Dependent Mechanisms J. Am. Soc. Nephrol., November 1, 2005; 16(11): 3222 - 3234. [Abstract] [Full Text] [PDF]