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  • Title: Effect of AT1R knockdown on ishikawa cell proliferation induced by estrogen.
    Author: Yang Q, Su Q, Wang G, Bi F, Sa R.
    Journal: Arch Gynecol Obstet; 2012 Aug; 286(2):481-7. PubMed ID: 22484478.
    Abstract:
    OBJECTIVE: This study aimed to study the effects of angiotensin receptor (AT1R) on proliferation, cell cycle progression, and apoptosis of estrogen-induced ishikawa cell by the transfection of AT1R-siRNA. METHODS: Immunofluorescence method was used to detect AT1R in ishikawa cell. Western blot was used to detect the expression of AT1R protein in ishikawa cell before and after the transfection of AT1R-siRNA. MTT method was used to test the cell proliferation of estrogen-induced ishikawa cell before and after the transfection. Western blot was used to detect the expression of extracellular regulated protein kinase1/2(ERK1/2). RESULTS: The result of immunofluorescence shows that AT1R was expressed in ishikawa cell. The expression of AT1R protein was inhibited obviously by 72 h after the transfection of AT1R-siRNA. The results of MTT show that estrogen could induce the cell proliferation of ishikawa cell. The expression of ERK1/2 was down-regulated after the transfection of AT1R-siRNA. CONCLUSION: AT1R can promote the cell proliferation of estrogen-induced ishikawa cell. The possible mechanism may be down-regulating the expression of ERK1/2 protein.
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