Regulation of growth-regulated oncogene alpha expression by estrogen in human endothelial cells
Abstract
Aim: To study the effect of estrogen on expression of growth-regulated oncogene alpha (GROalpha) in human umbilical vein endothelial cells (HUVEC) in vitro.
Methods: Expressions of CXC chemokine GROalpha mRNA and protein were measured by Northern blotting assay and ELISA, respectively. The physiological significance of GROalpha expression was tested by static cell adhesion assay.
Results: Both the GROalpha mRNA and protein levels decreased markedly after HUVEC were exposured to 17beta-estradiol (2 0.05 micromol/L. Moreover, the inhibition of the protein was depended on the concentration of 17beta-estradiol. Tamoxifen (0.1 micromol/L), an estrogen receptor alpha antagonist, alone did not affect GROalpha protein expression, but can reverse the E2 -induced inhibition of GROalpha protein expression (by up to 50 %) and the binding of U937 cells to E2-treated HUVEC (by up to 40 %).
Conclusion: Estrogen might functionally down-regulates GROalpha expression through estrogen receptor alpha on endothelial cells.
Keywords:
Methods: Expressions of CXC chemokine GROalpha mRNA and protein were measured by Northern blotting assay and ELISA, respectively. The physiological significance of GROalpha expression was tested by static cell adhesion assay.
Results: Both the GROalpha mRNA and protein levels decreased markedly after HUVEC were exposured to 17beta-estradiol (2 0.05 micromol/L. Moreover, the inhibition of the protein was depended on the concentration of 17beta-estradiol. Tamoxifen (0.1 micromol/L), an estrogen receptor alpha antagonist, alone did not affect GROalpha protein expression, but can reverse the E2 -induced inhibition of GROalpha protein expression (by up to 50 %) and the binding of U937 cells to E2-treated HUVEC (by up to 40 %).
Conclusion: Estrogen might functionally down-regulates GROalpha expression through estrogen receptor alpha on endothelial cells.