Inhibition of cell proliferation in the embryonic myocardium by A1 adenosine receptor activation
Article first published online: 17 APR 2001
Copyright © 2001 Wiley-Liss, Inc.
Volume 221, Issue 2, pages 194–200, June 2001
How to Cite
Zhao, Z. and Rivkees, S. A. (2001), Inhibition of cell proliferation in the embryonic myocardium by A1 adenosine receptor activation. Dev. Dyn., 221: 194–200. doi: 10.1002/dvdy.1130
- Issue published online: 16 MAY 2001
- Article first published online: 17 APR 2001
- Manuscript Accepted: 1 FEB 2001
- Manuscript Received: 10 APR 2000
- NIH. Grant Number: RO1-HL58442
- Patrick and Catherine Weldon Donaghue Medical Research Foundation
- A1 adenosine receptor;
- cell division;
A1 adenosine receptors (A1ARs) are expressed in the embryonic heart and influence cardiac function at early developmental stages. To test if A1ARs also affect cardiac structural development, we examined the effects of A1AR activation on heart formation. When pregnant mice were treated with the A1AR agonist, N6-cyclopentyladenosine (CPA), fetuses showed marked reduction of ventricular size and manifested features of heart failure. Suggesting that these findings represent direct effects on embryos, CPA treatment of cultured whole murine embryos resulted in cardiac hypoplasia. When rates of cell division and cell death in the heart were examined, we found decreases in cardiac cell proliferation following A1AR activation. In contrast, no changes in numbers or distribution of apoptotic cells were seen. Collectively, these data show that A1AR activation inhibits cardiac cell proliferation and can lead to cardiac hypoplasia. These data identify adenosine as a potential regulator of cardiac cell division during early development. © 2001 Wiley-Liss, Inc.