(Hypertension. 2000;36:330.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Angiotensin II Activates Collagen I Gene Through a Mechanism Involving the MAP/ER Kinase Pathway
From INSERM U.489, Hôpital Tenon, Paris, France (P.-L.T., C.C., F.F.), and AP-HP, Laboratoire de Physiologie, UFR St Antoine, Paris (J.-C.D.).
Correspondence to Jean-Claude Dussaule, MD, AP-HP, Laboratoire de Physiologie, UFR St Antoine, Paris 75012, France. E-mail jean-claude.dussaule{at}sat.ap-hop-paris.fr
Abstract—Vascular remodeling and
rearrangement of the extracellular matrix formation are among the major
adaptive mechanisms to chronic increase in blood pressure. In previous
studies we have found that angiotensin II (Ang II)
participates in the hypertension-associated aortic and renal vascular
fibrosis by stimulating collagen type I formation. The purpose of the
present study was to gain insight into the molecular events that
lead from the Ang II receptor to collagen I gene activation. To this
end, we used a novel strain of transgenic mice harboring the luciferase
gene under the control of the collagen I-
2 chain
promoter [procol2(I)]. Ang II produced an early (1
hour) 2- to 3-fold stimulation of procol2(I) activity in
freshly isolated aortas and renal cortical slices
(P<0.01) followed by similar increase in
procol2(I) mRNA aortic levels. This effect of Ang II was
inhibited by AT1-receptor antagonism (candesartan) and blockade of the
MAPK/ERK cascade (PD98059); in contrast, inhibition of the P38 kinase
pathway (SB202190) and blockade of the release of the transcription
factor NF
B (PDTC) did not have any effect in the Ang II–induced
activation of the collagen I gene. In addition, Ang II induced a rapid
(5 minutes) increase of the MAPK/ERK activity that was accompanied by
increased expression (3-fold) of the c-fos
proto-oncogene. This increase of c-fos mRNA expression
was blocked by PD98059; in addition, curcumin, a blocker of the
transcriptional factor AP-1, canceled the effect of Ang II on the
collagen I gene. Decorin, a scavenger of the active form of
transforming growth factor-ß (TGF-ß), canceled the Ang II effect on
collagen I gene, whereas inhibition of the MAPK/ERK pathway had no
effect on the TGF-ß–induced activation of procol2(I).
These data indicate that the cellular events after AT1 receptor
stimulation and leading to activation of collagen I gene expression
require activation of both the MAPK/ERK and TGF-ß signaling
pathways.
Key Words: collagen • angiotensin II • fibrosis • kinase • extracellular matrix • transforming growth factors
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