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1 Chicago College of Osteopathic Medicine, Downers Grove, Illinois 60551; 2 Department of Physiology, Michigan State University, East Lansing, Michigan 48824; and 3 Abbott Laboratories, Abbott Park, Waukegan, Illinois 60085
Previous work from this laboratory
demonstrated induction of apoptosis in lung alveolar epithelial
cells (AEC) by purified angiotensin II (ANG II) and expression of mRNAs
for both ANG II receptor subtypes AT1 and AT2
(Wang R, Zagariya A, Ibarra-Sunga O, Gidea C, Ang E, Deshmukh S,
Chaudhary G, Baraboutis J, Filippatos G, and Uhal BD. Am J
Physiol Lung Cell Mol Physiol 276: L885-L889, 1999.). The
present study was designed to determine the ANG II receptor subtype
mediating AEC apoptosis in response to ANG II. Apoptosis was induced with purified ANG II applied to the human lung AEC-derived carcinoma cell line A549 or to primary AEC isolated from Wistar rats. In both cell types, the AT1-selective
receptor antagonists L-158809 or losartan inhibited ANG II-induced
apoptosis by 90% at concentrations of 10
8 M and
107 M, respectively. The inhibition was concentration
dependent with IC50 of 1012 M and
1011 M on the primary rat AEC. In contrast, the
AT2-selective antagonists PD-123319 or PD-126055
could not block ANG II-induced apoptosis in either cell type.
In primary rat AEC, apoptosis in response to ANG II was blunted
in a dose-dependent manner by the protein kinase C inhibitor
chelerythrine but not by the tyrosine phosphatase inhibitor sodium
orthovanadate. Together, these data indicate that AEC apoptosis
in response to ANG II is mediated by receptor subtype AT1,
despite the expression of mRNAs for both AT1 and AT2.
type II pneumocyte; programmed cell death; angiotensin-converting enzyme inhibitor; pulmonary fibrosis; lung injury; angiotensin II
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