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J. Biol. Chem., Vol. 282, Issue 38, 28175-28188, September 21, 2007

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Chemerin, a Novel Adipokine That Regulates Adipogenesis and Adipocyte Metabolism^*

Kerry B. Goralski¹, Tanya C. McCarthy², Elyisha A. Hanniman³, Brian A. Zabel^¶||4, Eugene C. Butcher^¶||4, Sebastian D. Parlee, Shanmugam Muruganandan, and Christopher J. Sinal⁵

From the Department of Pharmacology and College of Pharmacy, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada, the ^¶Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, and ^||Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304

Obesity is an alarming primary health problem and is an independent risk factor for type II diabetes, cardiovascular diseases, and hypertension. Although the pathologic mechanisms linking obesity with these co-morbidities are most likely multifactorial, increasing evidence indicates that altered secretion of adipose-derived signaling molecules (adipokines; e.g. adiponectin, leptin, and tumor necrosis factor ) and local inflammatory responses are contributing factors. Chemerin (RARRES2 or TIG2) is a recently discovered chemoattractant protein that serves as a ligand for the G protein-coupled receptor CMKLR1 (ChemR23 or DEZ) and has a role in adaptive and innate immunity. Here we show an unexpected, high level expression of chemerin and its cognate receptor CMKLR1 in mouse and human adipocytes. Cultured 3T3-L1 adipocytes secrete chemerin protein, which triggers CMKLR1 signaling in adipocytes and other cell types and stimulates chemotaxis of CMKLR1-expressing cells. Adenoviral small hairpin RNA targeted knockdown of chemerin or CMKLR1 expression impairs differentiation of 3T3-L1 cells into adipocytes, reduces the expression of adipocyte genes involved in glucose and lipid homeostasis, and alters metabolic functions in mature adipocytes. We conclude that chemerin is a novel adipose-derived signaling molecule that regulates adipogenesis and adipocyte metabolism.

Received for publication, January 26, 2007 , and in revised form, June 18, 2007.

^* This work was supported in part by a Canadian Institutes of Health Research operating grant. 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. 1-3 and Table 1.

¹ Supported by postdoctoral fellowships from Canadian Institutes of Health Research, the IWK Health Centre, and the Reynolds Foundation.

² Supported by Graduate Student Scholarships from the Nova Scotia Health Research Foundation and the Canadian Institutes of Health Research.

³ Supported by a Graduate Student Scholarship from the Nova Scotia Health Research Foundation.

⁴ Supported by National Institutes of Health Grant AI-59635.

⁵ To whom correspondence should be addressed: Dept. of Pharmacology, Dalhousie University, Rm. 5E, Sir Charles Tupper Bldg., 5850 College St., Halifax, Nova Scotia B3H 1X5, Canada. Tel.: 902-494-2347; Fax: 902-494-1388; E-mail: csinal{at}dal.ca.

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