(Hypertension. 1999;33:1414-1419.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From Cardiovascular Research, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Masatsugu Horiuchi, MD, PhD, Department of Medical Biochemistry, Ehime University School of Medicine, Sigenobu, Onsen-gun, Ehime 791-0295, Japan. E-mail horiuchi{at}m.ehime-u.ac.jp
AbstractThe
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 receptornull mice.
-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
-smooth muscle actin
expression was observed between the wild-type and AT2
receptornull 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 receptornull 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.
Key Words: angiotensin cell differentiation receptors, angiotensin II muscle, smooth, vascular human development
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