The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/11/1615/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 9, November 3, 1997 1615-1620

Brief Definitive Reports

Wound Healing Is Accelerated by Agonists of Adenosine A2 (G{alpha}s-linked) Receptors

M. Carmen Montesinos*, Pratap Gadangi{ddagger}, Michael Longaker{ddagger}, Joanne Sung{ddagger}, Jamie Levine{ddagger}, Diana Nilsen*, Joan Reibman*, Min Li*, Chuan-Kui Jiang*, Rochelle Hirschhorn*, Phoebe A. Recht*,§, Edward Ostad*, Richard I. Levin*, and Bruce N. Cronstein*

From the * Department of Medicine; the {ddagger} Department of Surgery; and the § Laboratory for Cardiovascular Research, New York University Medical Center, New York 10016

The complete healing of wounds is the final step in a highly regulated response to injury. Although many of the molecular mediators and cellular events of healing are known, their manipulation for the enhancement and acceleration of wound closure has not proven practical as yet. We and others have established that adenosine is a potent regulator of the inflammatory response, which is a component of wound healing. We now report that ligation of the G{alpha}s-linked adenosine receptors on the cells of an artificial wound dramatically alters the kinetics of wound closure. Excisional wound closure in normal, healthy mice was significantly accelerated by topical application of the specific A2A receptor agonist CGS-21680 (50% closure by day 2 in A2 receptor antagonists. In rats rendered diabetic (streptozotocin-induced diabetes mellitus) wound healing was impaired as compared to nondiabetic rats; CGS-21680 significantly increased the rate of wound healing in both nondiabetic and diabetic rats. Indeed, the rate of wound healing in the CGS-21680–treated diabetic rats was greater than or equal to that observed in untreated normal rats. These results appear to constitute the first evidence that a small molecule, such as an adenosine receptor agonist, accelerates wound healing in both normal animals and in animals with impaired wound healing.

Address correspondence to Dr. B.N. Cronstein, Department of Medicine, NYU Medical Center, 550 1st Ave., New York, NY 10016. Phone: 212-263-6404; FAX: 212-263-8804; E-mail: cronsb01{at}mcrcr6.med.nyu.edu


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