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J. Biol. Chem., Vol. 279, Issue 27, 28670-28674, July 2, 2004

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Adiponectin Stimulates Angiogenesis in Response to Tissue Ischemia through Stimulation of AMP-activated Protein Kinase Signaling^*

Rei Shibata¶, Noriyuki Ouchi¶, Shinji Kihara||, Kaori Sato, Tohru Funahashi||, and Kenneth Walsh**

From the Molecular Cardiology/Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118 and ^||Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2, Yamada-oka, Suita, Osaka, 565-0871, Japan

Obesity is a risk factor for the development of cardiovascular diseases that are associated with impaired angiogenesis. Adiponectin is an adipocyte-specific adipocytokine with anti-atherogenic and anti-diabetic properties, and its plasma levels are reduced in association with obesity-linked diseases. Here, we investigated whether adiponectin regulates angiogenesis in response to tissue ischemia using adiponectin knock-out (KO) mice. Angiogenic repair of ischemic hind limbs was impaired in adiponectin-KO mice compared with wild-type (WT) mice as evaluated by laser Doppler flow method and capillary density analyses. Adenovirus-mediated supplement of adiponectin accelerated angiogenic repair in both adiponectin-KO and WT mice. Intramuscular injection of an adenovirus encoding dominant-negative AMP-activated kinase diminished the improvement in limb perfusion seen in WT mice and abolished the adiponectin-induced enhancement of perfusion. These data indicate that adiponectin can function to stimulate angiogenesis in response to ischemic stress by promoting AMP-activated kinase signaling. Therefore, adiponectin may be useful in the treatment for obesity-related vascular deficiency diseases.

Received for publication, March 5, 2004 , and in revised form, April 12, 2004.

^* This work was supported by National Institutes of Health Grants AR40197, HD23681, AG15052, and AG17241 (to K. W.) and by grants from the Japanese Ministry of Education and the Japan Society for Promotion of Science-Research for the Future Program. 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.

These authors contributed equally to this work.

^¶ Supported by grants from the Uehara Memorial Foundation.

^** To whom correspondence should be addressed: Molecular Cardiology/Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany St., W611, Boston, MA 02118. Tel.: 617-414-2390; Fax: 617-414-2391; E-mail: kxwalsh{at}bu.edu.

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