Effects of Raloxifene on Caveolin-1 mRNA and Protein Expressions in Vascular Smooth Muscle Cells

来源 :Acta Biochimica et Biophysica Sinica | 被引量 : 0次 | 上传用户:leeo_1987
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Caveolin-1 is regulated by estrogen in vascular smooth muscle cells.Raloxifene,a selectiveestrogen receptor modulator that possibly has cardioprotective properties without an increased risk of canceror other side effects of estrogen,may be used in women with risk of coronary artery disease.However,therelationship between raloxifene and caveolin-1 is still unknown.Therefore,this study was designed to seewhether raloxifene regulates caveolin-1 expression and if so,whether such regulation is mediated by estrogenreceptor.Rat aortic smooth muscle cells were cultured in the absence or presence of raloxifene (10~(-8) to10~(-6) M) for 12 or 24 h.Both mRNA and protein levels of caveolin-1 were increased significantly after 24 htreatment with raloxifene.These increases were inhibited by estrogen receptor antagonist ICI 182780 (10~(-5)M).Results of this study suggest that raloxifene stimulates caveolin-1 transcription and translation throughestrogen receptor mediated mechanisms. Caveolin-1 is regulated by estrogen in vascular smooth muscle cells. Raloxifene, a selectiveestrogen receptor modulator that has has cardioprotective properties without an increased risk of canceror other side effects of estrogen, may be used in women with risk of coronary artery disease. However, therelationship between raloxifene and caveolin-1 is still unknown. Before, this study was designed to see whether raloxifene regulates caveolin-1 expression and if so, whether such regulation is mediated by estrogen receptor. Rat aortic smooth muscle cells were cultured in the absence or presence of raloxifene (10 ~ (-8) to10 ~ (-6) M) for 12 or 24 h.Both mRNA and protein levels of caveolin-1 were increased significantly after 24 h treatment with raloxifene. These sesections were inhibited by estrogen receptor antagonist ICI 182780 (10 ~ (-5) M). Results of this study suggest that raloxifene stimulates caveolin-1 transcription and translation throughestrogen receptor mediated mechanisms.
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