Abstract:

Objective    To explore the effects and mechanism of the estrogen receptor on stressinduced premature senescence of vascular smooth muscle cells (VSMCS). Methods     The VSMCS, cultured from female SD rats and followed by 23 vitro passages , were induced into senescence by exposure to 150μmol/L H2O2 in the presence or absence of different concentrations (10-10mol/L-10-8mol/L) of PPT/DPN. Expressions of senescence associated marker (DcR2) were detected by flow cytometry. Expressions or activities of the protooncogene Ras were detected by pull-down assay and Western blotting analysis.   Results     Flow cytometry analysis showed that in physiological concentrations, the estrogen receptor agonist significantly inhibited H2O2promoted highlevel expression of DcR2 of VSMCS in a dosedependent manner（P﹤0.05）. Pulldown assay and Western blotting analysis revealed that administration of (10-10mol/L-10-8mol/L) of PPT/DPN obviously reduced the H2O2-induced activity of Ras（P﹤0.05）.  Conclusion     The estrogen receptor exerts inhibitive effect on stress-induced senescence of VSMCS by suppressing activity of Ras. ERa and ERb may have the same effects on stress-induced premature senescence of vascular smooth muscle cells in vitro.

Key words: Estrogen receptor； Vascular smooth muscle cells； Stress inducedsenescence