期刊
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
卷 115, 期 1-2, 页码 36-43出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2009.02.014
关键词
Progesterone; Endothelial cell; Cell proliferation; Protein kinase C; Nitric oxide; Cell migration
资金
- Universtdad Nacional del Sur, Argentina [PGI 24/BO93]
- Agencia Nacional de Promocion Cientifica [PICTO 527]
We tested the hypothesis whether; the non-genomic action of progesterone (Pg) on vascular tissue would be associated with hormonal long term effect on the modulation of cell growth. Using rat aortic strips, we showed that the stimulatory effect of Pg on nitric oxide synthesis involved both kinase and phosphatase pathways. The increase in the vasoactive production was prevented by the MAPK inhibitor (PD98059). In addition, preincubation with a phosphatase antagonist potentiated the hormonal effect. Pg increased PKC activity, but the inhibition of PKC did not alter the stimulatory action of the hormone on nitric oxide generation. In endothelial cell cultures (EC), 24 h treatment with Pg significantly diminished cell proliferation. This antiproliferative effect was suppressed by the PKC inhibitor chelerythrine (chel) and L-NAME (nitric oxide synthase inhibitor). We also observed that Pg stimulates EC migration. In summary, the present findings provide evidence of an integration of genomic and non-genomic effects in the mechanism of action displayed by Pg in vascular tissue. The fast effects elicited by the hormone implies signal transduction activation required for the regulation of vasoactive production, but also necessary for the modulation of endothelial cells growth. (c) 2009 Elsevier Ltd. All rights reserved.
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