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1 Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, Korea, Republic of
2 Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, Japan
* To whom correspondence should be addressed. E-mail: hiito{at}kuhp.kyoto-u.ac.jp.
Both nitric oxide (NO) and natriuretic peptides produce apoptosis of vascular smooth muscle cells. However, there is evidence that NO induces endothelial cell proliferation, which suggests there is a difference in the response of endothelial cells to natriuretic peptides. The purpose of this study was to investigate the effect of atrial natriuretic peptide (ANP) on the human endothelial cell survival. ANP within the physiological concentration (10-11 mol/L) induced a 52% increase in number of human coronary arterial endothelial cells (HCAEC) and a 63% increase in human umbilical vein endothelial cells (HUVEC) at a low concentration of serum. The increase in cell numbers was blocked by pretreatment with RP8-CPT-cGMP (RP8), a cGMP-dependent protein kinase (cGK) inhibitor, with Wortmannin, an Akt/PKB inhibitor, and with PD98059, an Erk 1/2 inhibitor. In a Transwell migration test, ANP also increased the cell migration and RP8, Wortmannin, and PD98059 blocked this increase. A wound healing assay was performed to examine the effects of ANP on regeneration in vitro. ANP increased both cell numbers and migration, but the effects were blocked by the above three kinase inhibitors. ANP increased the expression of phospho-Akt within 1.5 h and of phospho-Erk 1/2. These results suggest that ANP can potentiate endothelial regeneration by cGK stimulation and subsequent Akt and Erk 1/2 activations.
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