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(Circulation Research. 2008;102:280.)
© 2008 American Heart Association, Inc.

Editorials

Adenosine Prompts the Heart to Recruit Endothelial Progenitors

Jianzhong Shen, Paul E. DiCorleto

From the Department of Cell Biology, The Lerner Research Institute, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic Foundation, Ohio.

Correspondence to Jianzhong Shen, PhD, Department of Cell Biology, The Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail shenj@ccf.org

See related article, pages 356–363

Key Words: adenosine • endothelial progenitor cells • receptors • microvasculature

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Adenosine has a long history of involvement in cardiac function. It was first purified from mammalian heart homogenates in 1929 by Drury and Szent-Györgyi,¹ who reported a "suppressive" action of adenosine on the heart, including decreased heart beat rate and perfusion pressure,¹ now termed bradycardia and coronary artery vasodilation, respectively. Based on a variety of experimental results from several laboratories, Berne et al proposed in the early 1960s that adenosine plays an important role in the adjustment of blood flow to the metabolic requirements of organs, including the heart, brain, and skeletal muscle.² Numerous studies now support the hypothesis that adenosine can be directly released or generated from released ATP/ADP in the heart during ischemia, causing increased oxygen and nutrition supply by inducing coronary artery relaxation.³

Although adenosine exhibits reuptake via specific adenosine transporters, many, if not all, of the biological effects of adenosine are believed to be mediated by adenosine receptors (ARs), of which 4 subtypes (A₁R, A_2AR, A_2BR, and A₃R) have been cloned and pharmacologically characterized.⁴ The diverse physiological functions mediated by the different AR subtypes, particularly in the modulation of the cardiovascular system, have been confirmed by genetically engineered mice.⁴ Null mice have been generated for each of the AR subtypes, and none of the 4 ARs plays a critical role during development.^4,5 Although each AR protein had been thought to exist in the cell membrane as a monomer, recent studies with recombinant expression systems have revealed that some of the AR subtypes . . . [Full Text of this Article]

Related Article:

Adenosine Receptor–Mediated Adhesion of Endothelial Progenitors to Cardiac Microvascular Endothelial Cells

Sergey Ryzhov, Nataliya V. Solenkova, Anna E. Goldstein, Mathias Lamparter, Todd Fleenor, Pampee P. Young, James P. Greelish, John G. Byrne, Douglas E. Vaughan, Italo Biaggioni, Antonis K. Hatzopoulos, and Igor Feoktistov
Circ. Res. 2008 102: 356-363. [Abstract] [Full Text] [PDF]

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