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Departments of 1 Diabetes and 2 Molecular Biology, Beckman Research Institute of the City of Hope, Duarte 91010; 4 Division of Nephrology, Harbor-UCLA Research and Education Institute, Torrance, California 90509; and 3 Department of Endocrinology, University of Virginia Medical School, Charlottesville, Virginia 22908
The lipoxygenase (LO) pathway of
arachidonate metabolism and mitogen-activated protein kinases (MAPKs)
can mediate cellular growth and ANG II effects in vascular smooth
muscle cells. However, their role in renal mesangial cells (MC) is not
very clear. ANG II treatment of rat MC significantly increased 12-LO
mRNA expression and formation of the 12-LO product
12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE;
P < 0.03]. ANG II-induced [3H]leucine
incorporation was blocked by an LO inhibitor,
cinnamyl-3,4-dihydroxy-
-cyanocinnamate (P < 0.02).
12(S)-HETE and ANG II directly induced cellular hypertrophy and fibronectin (FN) expression (P < 0.01) to a
similar extent. ANG II and 12(S)-HETE led to activation of
p38MAPK and its target transcription factor cAMP-responsive
element-binding protein (CREB). ANG II- and
12(S)-HETE-induced CREB activation and
[3H]leucine incorporation were blocked by the
p38MAPK inhibitor SB-202190. A specific molecular inhibitor
of rat 12-LO mRNA, namely, a novel ribozyme, could attenuate ANG
II-induced FN mRNA. Thus p38MAPK-dependent CREB activation
may mediate ANG II- and LO product-induced FN expression and cellular
growth in rat MC. ANG II effects may be mediated by the LO pathway.
These results suggest a novel interaction between LO and
p38MAPK activation in MC matrix synthesis associated with
renal complications.
angiotensin II; 12(S)-hydroxyeicosatetraenoic acid; hypertrophy; p38MAPK; cAMP-responsive element-binding protein; fibronectin; rat
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