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P-糖蛋白通过增强氯离子通道-3的磷酸化介导术后腹膜粘连形成。

P-glycoprotein Mediates Postoperative Peritoneal Adhesion Formation by Enhancing Phosphorylation of the Chloride Channel-3.

作者信息

Deng Lulu, Li Qin, Lin Guixian, Huang Dan, Zeng Xuxin, Wang Xinwei, Li Ping, Jin Xiaobao, Zhang Haifeng, Li Chunmei, Chen Lixin, Wang Liwei, Huang Shulin, Shao Hongwei, Xu Bin, Mao Jianwen

机构信息

1. Guangdong Provincial Key Laboratory of pharmaceutical Bioactive Substances and School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou 510006, China.

1. Guangdong Provincial Key Laboratory of pharmaceutical Bioactive Substances and School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou 510006, China; 7. The People's Hospital of Liupanshui City, Liupanshui 553001, China.

出版信息

Theranostics. 2016 Jan 1;6(2):204-18. doi: 10.7150/thno.13907. eCollection 2016.

Abstract

P-glycoprotein (P-gp) is encoded by the multidrug resistance (MDR1) gene and is well studied as a multi-drug resistance transporter. Peritoneal adhesion formation following abdominal surgery remains an important clinical problem. Here, we found that P-gp was highly expressed in human adhesion fibroblasts and promoted peritoneal adhesion formation in a rodent model. Knockdown of P-gp expression by intraperitoneal injection of MDR1-targeted siRNA significantly reduced both the peritoneal adhesion development rate and adhesion grades. Additionally, we found that operative injury up-regulated P-gp expression in peritoneal fibroblasts through the TGF-β1/Smad signaling pathway and histone H3 acetylation. The overexpression of P-gp accelerated migration and proliferation of fibroblasts via volume-activated Cl(-) current and cell volume regulation by enhancing phosphorylation of the chloride channel-3. Therefore, P-gp plays a critical role in postoperative peritoneal adhesion formation and may be a valuable therapeutic target for preventing the formation of peritoneal adhesions.

摘要

P-糖蛋白(P-gp)由多药耐药(MDR1)基因编码,作为一种多药耐药转运蛋白已得到充分研究。腹部手术后腹膜粘连的形成仍然是一个重要的临床问题。在此,我们发现P-gp在人粘连成纤维细胞中高表达,并在啮齿动物模型中促进腹膜粘连的形成。通过腹腔注射靶向MDR1的小干扰RNA(siRNA)敲低P-gp表达,可显著降低腹膜粘连的发生率和粘连分级。此外,我们发现手术损伤通过转化生长因子-β1(TGF-β1)/Smad信号通路和组蛋白H3乙酰化上调腹膜成纤维细胞中P-gp的表达。P-gp的过表达通过增强氯离子通道-3的磷酸化,经由容积激活的Cl(-)电流和细胞容积调节,加速成纤维细胞的迁移和增殖。因此,P-gp在术后腹膜粘连形成中起关键作用,可能是预防腹膜粘连形成的一个有价值的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c630/4729769/a4cb24377883/thnov06p0204g001.jpg

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