Estrogen, but not androgen, inhibits the proliferation of cultured vascular smooth muscle cells derived from male and female spontaneously hypertensive rats

Academic Article


  • Our previous studies demonstrated that myointimal proliferation after balloon injury of the carotid artery is significantly decreased in female spontaneously hypertensive rats (SHR) compared to age matched males, and that the gender difference in myointimal proliferation is estrogen dependent. In the present study we used cultured vascular smooth muscle cell (VSMC) to determine the cellular mechanism of this response. VSMC were derived from thoracic aortae of 8 wks old male and female SHR. VSMC in passage 3 were cultured in serum-free medium for 48 hrs and then, grown in steroid-free medium for 4-5 days with or without adding 17β-estradiol(E2, 10-1000nM). Cell numbers were counted using hemacytometer. Results (means±SE) expressed as % over control values are: Control 10nM 100nM 1000nM (n=7) 100% 95.8±2.6% 91.5±5.1% 83.1±6.5% * (n=7) 100% 95.5±2.0% 88.7±2.3%* 77.2±3.8% * * p<0.01, compared to their controls. There was no gender difference in the growth rate of the control or E2-treated VSMC. E2 induced a dose-dependent reduction in VSMC growth that was confirmed by [3H]-hymidine incorporation. In a parallel experiment, we found that dihydrotestosterone (1-1000nM) had no effect on VSMC growth or [3H]-thymidine incorporation in either sexes. These findings indicate that E2 directly inhibits VSMC proliferation in both sexes. This mechanism is likely responsible for the sexual dimorphism of restenosis after vascular injury in vivo.
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  • Tang W; Chen YF; Oparil S
  • Volume

  • 44
  • Issue

  • 1