AT2 receptor and vascular smooth muscle cell differentiation in vascular development.

Published

Journal Article

The angiotensin II type 2 (AT2) receptor is transiently expressed at late gestation in the fetal vasculature, but its expression rapidly declines after birth. We have previously demonstrated that the expression of this receptor mediates decline in vascular DNA synthesis that occurs at this stage of vascular development. To examine further the role of the AT2 receptor in vasculogenesis, we have focused on the effect of the AT2 receptor on vascular smooth muscle cell (VSMC) differentiation. In this study, we examined the time-dependent expression of differentiation markers for VSMCs in the aorta of wild-type and AT2 receptor-null mice. alpha-Smooth muscle actin was expressed at the early stage of differentiation and exhibited unchanged expression before and after the peak of AT2 receptor expression, which was observed at embryonic day 20, neonatal day 1, and thereafter. No difference in alpha-smooth muscle actin expression was observed between the wild-type and AT2 receptor-null mice. In contrast, the mRNA levels for calponin, expressed in the late stage of VSMC differentiation, were significantly higher in the wild-type mouse aorta as compared with the AT2 receptor-null mice, which correlates with expression of the AT2 receptor. Moreover, the protein levels of calponin and high-molecular-weight caldesmon (h-caldesmon) showed lower expression in the aorta of AT2 receptor knockout mice at 2 and 4 weeks after birth. Taken together, our results suggest that the AT2 receptor promotes vascular differentiation and contributes to vasculogenesis.

Full Text

Duke Authors

Cited Authors

  • Yamada, H; Akishita, M; Ito, M; Tamura, K; Daviet, L; Lehtonen, JY; Dzau, VJ; Horiuchi, M

Published Date

  • June 1999

Published In

Volume / Issue

  • 33 / 6

Start / End Page

  • 1414 - 1419

PubMed ID

  • 10373225

Pubmed Central ID

  • 10373225

International Standard Serial Number (ISSN)

  • 0194-911X

Digital Object Identifier (DOI)

  • 10.1161/01.hyp.33.6.1414

Language

  • eng

Conference Location

  • United States