本文選題：轉(zhuǎn)化生長因子β + 人支氣管上皮細(xì)胞��； 參考：《中國病理生理雜志》2017年06期

【摘要】：目的:探究小窩蛋白1(caveolin-1)在轉(zhuǎn)化生長因子β1(TGF-β1)誘導(dǎo)的人支氣管上皮細(xì)胞(16HBE細(xì)胞)上皮-間充質(zhì)轉(zhuǎn)化(EMT)中的作用。方法:以16HBE細(xì)胞株為研究對象,免疫熒光、RT-q PCR和Western blot實驗檢測16HBE細(xì)胞EMT過程中caveolin-1的mRNA和蛋白表達(dá);Western blot檢測siRNA干擾caveolin-1對16HBE細(xì)胞EMT的影響。結(jié)果:Caveolin-1廣泛存在于16HBE細(xì)胞膜上,TGF-β1刺激后,caveolin-1的mRNA和蛋白表達(dá)減少(P0.05)。與TGF-β1組比較,caveolin-1 siRNA和TGF-β1共同作用促進(jìn)了細(xì)胞形態(tài)的轉(zhuǎn)化,抑制了E-鈣黏蛋白的蛋白表達(dá)而促進(jìn)了α-SMA的蛋白表達(dá)(P0.05)。TGF-β1刺激16HBE細(xì)胞后,AKT和Smad3在30 min磷酸化水平最高,與0 min對照組比較顯著增加(P0.05);用siRNA干擾caveolin-1基因后再用TGF-β1刺激16HBE細(xì)胞30 min,下游信號蛋白分子AKT和Smad3的磷酸化水平增高,與TGF-β1組比較顯著增加(P0.05)。結(jié)論:TGF-β1能下調(diào)16HBE細(xì)胞的caveolin-1表達(dá)水平;caveolin-1可能參與了TGF-β1誘導(dǎo)的16HBE細(xì)胞EMT過程中TGF-β1/Smad通路和PI3K-AKT通路的活化。
[Abstract]:Aim: to investigate the role of fossa protein 1 caveolin-1 in epithelial-mesenchymal transformation (EMTT) induced by transforming growth factor 尾 1 (TGF- 尾 1) in human bronchial epithelial cells (TGF- 尾 1). Methods: the expression of mRNA and protein of caveolin-1 in EMT of 16HBE cells was detected by immunofluorescence RT-q PCR and Western blot assay. The effect of siRNA interference caveolin-1 on EMT of 16HBE cells was detected by Western blot. Results the expression of mRNA and protein of TGF- 尾 1 in 16HBE cells was decreased after the stimulation of TGF- 尾 1. Compared with TGF- 尾 1 group, the co-action of TGF- 尾 1 siRNA and TGF- 尾 1 promoted the transformation of cell morphology, inhibited the protein expression of Ecadherin, and promoted the expression of 偽 -SMA protein. The phosphorylation levels of AK T and Smad3 in 16HBE cells stimulated by TGF- 尾 1 and TGF- 尾 1 were the highest at 30 min. Compared with 0 min control group, the level of phosphorylation of AKT and Smad3 increased significantly in 16HBE cells after siRNA interference with caveolin-1 gene and then stimulated with TGF- 尾 1 for 30 min, and the phosphorylation level of AKT and Smad3 increased significantly compared with TGF- 尾 1 group, and the phosphorylation level of TGF- 尾 1 increased significantly as compared with that of TGF- 尾 1 group. Conclusion: TGF- 尾 1 can down-regulate the expression of caveolin-1 in 16HBE cells. Caveolin-1 may be involved in the activation of TGF- 尾 1/Smad pathway and PI3K-AKT pathway in 16HBE cells induced by TGF- 尾 1.
【作者單位】： 廣州市花都區(qū)人民醫(yī)院;廣州醫(yī)科大學(xué)生理學(xué)教研室;黃石市中心醫(yī)院;
【基金】：國家自然科學(xué)基金資助項目(No.81470205)
【分類號】：R562.25

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