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Submitted on July 20, 2004
Accepted on November 4, 2004
Service of Endocrinology, Department of Medicine, and Department of Physiology and Biophysics, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, Quebec, Canada, J1H 5N4
* To whom correspondence should be addressed. E-mail: Nicole.Gallo-Payet{at}USherbrooke.ca.
Angiotensin II (Ang Il) is one of the most important stimuli of rat adrenal glomerulosa cells. The aim of the present study was to investigate whether Ang Il can stimulate cell proliferation and/or hypertrophy and to investigate pathways and intracellular targets. A three-day treatment with Ang II (5-100 nM), through the AT1 receptor subtype, abolished cell proliferation observed in control cells, but increased protein synthesis. Preincubation with PD98059 (a MEK inhibitor) abolished basal proliferation and had no effect on basal protein synthesis but did reverse the effect of Ang II on protein synthesis. The p38 MAPK inhibitor SB203580 reversed the inhibitory effect on cell proliferation and abolished the increase in protein synthesis, whereas the JNK inhibitor, SP600125 had no effect. Time-course studies revealed that Ang II stimulated phosphorylation of both p42/p44mapk and p38 MAPK, but did not activate JNK. Ang II had no effect on the level of cyclin E expression, but increased the expression of the cyclin-dependent kinase, p27Kip1, an effect abolished in cells preincubated with SB203580 and PD98059. In conclusion, in cultured rat glomerulosa cells, a three-day treatment with Ang II increases protein synthesis, with a concomitant decrease in proliferation. These effects are mediated by both the p42/p44mapk and the p38 MAPK pathways, which increase expression of the steroidogenic enzymes, StAR and 3
-HSD and of p27Kip1, a protein known to block the cell cycle in G1 phase. Together, these results support the key role of Ang II as a stimulus of steroid synthesis rather than a proliferating factor.
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