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本文引用的文献

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Constitutive modeling of the stress-strain behavior of F-actin filament networks.F-肌动蛋白丝网络应力-应变行为的本构模型。
Acta Biomater. 2008 May;4(3):597-612. doi: 10.1016/j.actbio.2007.12.007. Epub 2008 Jan 8.
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Low shear stress-induced interleukin-8 mRNA expression in endothelial cells is mechanotransduced by integrins and the cytoskeleton.低剪切应力诱导内皮细胞中白细胞介素-8信使核糖核酸表达是通过整合素和细胞骨架进行机械转导的。
Endothelium. 2007 Nov-Dec;14(6):265-73. doi: 10.1080/10623320701678169.
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Mechanical forces in diabetic kidney disease: a trigger for impaired glucose metabolism.糖尿病肾病中的机械力:葡萄糖代谢受损的诱因
J Am Soc Nephrol. 2007 Aug;18(8):2226-32. doi: 10.1681/ASN.2006121362. Epub 2007 Jul 18.
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Hydrostatic pressure influences morphology and expression of VE-cadherin of vascular endothelial cells.流体静压影响血管内皮细胞的形态和血管内皮钙黏蛋白的表达。
J Biomech. 2007;40(11):2399-405. doi: 10.1016/j.jbiomech.2006.11.023. Epub 2007 Jan 29.
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Molecular mechanisms of the vascular responses to haemodynamic forces.血管对血流动力学力反应的分子机制。
J Intern Med. 2006 Apr;259(4):381-92. doi: 10.1111/j.1365-2796.2006.01624.x.
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An introductory review of cell mechanobiology.细胞机械生物学导论综述
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TGF-beta and epithelial-to-mesenchymal transitions.转化生长因子-β与上皮-间质转化
Oncogene. 2005 Aug 29;24(37):5764-74. doi: 10.1038/sj.onc.1208927.
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Intermittent pressure-loading increases transforming growth factor-beta-1 secretion from renal tubular epithelial cells: in vitro vesicoureteral reflux model.
Urol Int. 2005;75(2):150-8. doi: 10.1159/000087170.
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Microfilaments are involved in renal cell responses to sustained hydrostatic pressure.微丝参与肾细胞对持续静水压力的反应。
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Chronic kidney disease: the global challenge.慢性肾脏病:全球面临的挑战。
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体外液压诱导肾小管上皮细胞-肌成纤维细胞转分化

Hydraulic pressure inducing renal tubular epithelial-myofibroblast transdifferentiation in vitro.

作者信息

Li Fei-yan, Xie Xi-sheng, Fan Jun-ming, Li Zi, Wu Jiang, Zheng Rong

机构信息

Department of Nephrology, West China Hospital of Sichuan University, Chengdu 610041, China.

出版信息

J Zhejiang Univ Sci B. 2009 Sep;10(9):659-67. doi: 10.1631/jzus.B0920110.

DOI:10.1631/jzus.B0920110
PMID:19735098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2738835/
Abstract

OBJECTIVE

The effects of hydraulic pressure on renal tubular epithelial-myofibroblast transdifferentiation (TEMT) were investigated.

METHODS

We applied hydraulic pressure (50 cm H2O) to normal rat kidney tubular epithelial cells (NRK52E) for different durations. Furthermore, different pressure magnitudes were applied to cells. The morphology, cytoskeleton, and expression of myofibroblastic marker protein and transforming growth factor-beta1 (TGF-beta1) of NRK52E cells were examined.

RESULTS

Disorganized actin filaments and formation of curling clusters in actin were seen in the cytoplasm of pressurized cells. We verified that de novo expression of alpha-smooth muscle actin induced by pressure, which indicated TEMT, was dependent on both the magnitude and duration of pressure. TGF-beta1 expression was significantly upregulated under certain conditions, which implies that the induction of TEMT by hydraulic pressure is related with TGF-beta1.

CONCLUSION

We illustrate for the first time that hydraulic pressure can induce TEMT in a pressure magnitude- and duration-dependent manner, and that this TEMT is accompanied by TGF-beta1 secretion.

摘要

目的

研究液压对肾小管上皮细胞-肌成纤维细胞转分化(TEMT)的影响。

方法

我们对正常大鼠肾小管上皮细胞(NRK52E)施加不同时长的液压(50 cm H2O)。此外,对细胞施加不同的压力大小。检测NRK52E细胞的形态、细胞骨架以及肌成纤维细胞标志物蛋白和转化生长因子-β1(TGF-β1)的表达。

结果

在受压细胞的细胞质中可见肌动蛋白丝排列紊乱以及肌动蛋白卷曲簇的形成。我们证实压力诱导的α-平滑肌肌动蛋白的从头表达表明了TEMT,其依赖于压力大小和时长。在某些条件下TGF-β1表达显著上调,这意味着液压诱导的TEMT与TGF-β1有关。

结论

我们首次表明液压能够以压力大小和时长依赖的方式诱导TEMT,并且这种TEMT伴随着TGF-β1的分泌。