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首页> 外文期刊>International journal of biological sciences >Cdc42-Interacting Protein-4 Promotes TGF-Β1-Induced Epithelial-Mesenchymal Transition and Extracellular Matrix Deposition in Renal Proximal Tubular Epithelial Cells
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Cdc42-Interacting Protein-4 Promotes TGF-Β1-Induced Epithelial-Mesenchymal Transition and Extracellular Matrix Deposition in Renal Proximal Tubular Epithelial Cells

机译：Cdc42相互作用蛋白4促进肾小管上皮细胞中TGF-β1诱导的上皮-间质转化和细胞外基质沉积。

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Cdc42-interacting protein-4 (CIP4) is an F-BAR (Fer/CIP4 and Bin, amphiphysin, Rvs) family member that regulates membrane deformation and endocytosis, playing a key role in extracellular matrix (ECM) deposition and invasion of cancer cells. These processes are analogous to those observed during the initial epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. The role of CIP4 in renal tubular EMT and renal tubulointerstitial fibrosis was investigated over the course of the current study, demonstrating that the expression of CIP4 increased in the tubular epithelia of 5/6-nephrectomized rats and TGF-β1 treated HK-2 cells. Endogenous CIP4 evidenced punctate localization throughout the cytosol, with elevated levels observed in the perinuclear region of HK-2 cells. Subsequent to TGF-β1 treatment, CIP4 expression increased, forming clusters at the cell periphery that gradually redistributed into the cytoplasm. Simultaneously, EMT induction in cells was confirmed by the prevalence of morphological changes, loss of E-cadherin, increase in α-SMA expression, and secretion of fibronectin. Overexpression of CIP4 promoted characteristics similar to those commonly observed in EMT, and small interfering RNA (siRNA) molecules capable of CIP4 knockdown were used to demonstrate reversed EMT. Cumulatively, results of the current study suggest that CIP4 promotes TGF-β1-induced EMT in tubular epithelial cells. Through this mechanism, CIP4 is capable of inducing ECM deposition and exacerbating progressive fibrosis in chronic renal failure.
机译：Cdc42相互作用蛋白4（CIP4）是F-BAR（Fer / CIP4和Bin，amphiphysin，Rvs）家族成员，可调节膜变形和内吞作用，在细胞外基质（ECM）沉积和癌细胞侵袭中发挥关键作用。这些过程类似于在肾小管上皮细胞的初始上皮-间质转化（EMT）期间观察到的过程。在当前研究过程中，研究了CIP4在肾小管EMT和肾小管间质纤维化中的作用，表明CIP4在5/6肾切除大鼠和TGF-β1处理的HK-2细胞的肾小管上皮中表达增加。内源性CIP4在整个胞质溶胶中均呈点状定位，在HK-2细胞的核周区域中观察到水平升高。 TGF-β1处理后，CIP4表达增加，在细胞周围形成簇，并逐渐重新分布到细胞质中。同时，通过形态变化的普遍性，E-钙黏着蛋白的丢失，α-SMA表达的增加以及纤连蛋白的分泌，证实了细胞中EMT的诱导。 CIP4的过表达促进了类似于EMT中通常观察到的特征，并且使用能够CIP4敲低的小干扰RNA（siRNA）分子来证明EMT反向。累积地，当前的研究结果表明，CIP4促进了TGF-β1诱导的肾小管上皮细胞的EMT。通过这种机制，CIP4能够在慢性肾衰竭中诱导ECM沉积并加重进行性纤维化。

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