Beta1 integrin-mediated adhesion between renal tubular cells after anoxic injury.

1997 ◽  
Vol 8 (2) ◽  
pp. 175-183
Author(s):  
W Lieberthal ◽  
J B McKenney ◽  
C R Kiefer ◽  
L M Snyder ◽  
V M Kroshian ◽  
...  
Keyword(s):  
Primary Cultures ◽  
Atp Depletion ◽  
Apical Surface ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Anoxic Injury ◽  
Sublethal Injury ◽  
Beta 1 Integrin ◽  
Renal Tubular ◽  
And Function

beta 1 integrin-mediated adhesion between renal tubular cells after anoxic injury. This study examined the effect of sublethal injury, induced by ATP depletion (5 mM cyanide in the absence of dextrose), on the distribution and function of beta 1 integrins in primary cultures of mouse proximal tubular (MPT) cells. It was shown in this study that sublethal injury results in loss of focal contacts present in uninjured MPT cells, and that the beta 1 integrin molecule becomes redistributed to the apical membrane domain of sublethally injured cells. Polystyrene beads coated with Arg-Gly-Asp (RGD)-containing peptide adhere to the surface of sublethally injured MPT cells but not to control, dextrose-treated cells, indicating that the beta 1 integrins present on the apical surface of the cell remain functional. The presence of an excess of free RGD-containing peptide reduces binding of RGD-coated beads to sublethally injured MPT cells by approximately 50%. It was also demonstrated that adherence of MPT cells in suspension to cyanide-treated monolayers is increased more than 300% above adhesion to control, uninjured monolayers. This abnormal cell-cell adhesion is ameliorated by the presence of an excess of RGD-containing peptide and is reversed if cyanide-treated cells are allowed to recover for 1 h. It was concluded that the beta 1 integrin becomes expressed on the apical surface of MPT cells after sublethal injury. These apically expressed integrins remain functional and mediate aberrant adhesion between MPT cells.

scholarly journals HIF-1-mediated production of exosomes during hypoxia is protective in renal tubular cells

2017 ◽  
Vol 313 (4) ◽  
pp. F906-F913 ◽  
Author(s):  
Wei Zhang ◽  
Xiangjun Zhou ◽  
Qisheng Yao ◽  
Yutao Liu ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Cell Injury ◽  
Hypoxia Inducible Factor ◽  
Atp Depletion ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Exosomes are nano-sized vesicles produced and secreted by cells to mediate intercellular communication. The production and function of exosomes in kidney tissues and cells remain largely unclear. Hypoxia is a common pathophysiological condition in kidneys. This study was designed to characterize exosome production during hypoxia of rat renal proximal tubular cells (RPTCs), investigate the regulation by hypoxia-inducible factor-1 (HIF-1), and determine the effect of the exosomes on ATP-depletion-induced tubular cell injury. Hypoxia did not change the average sizes of exosomes secreted by RPTCs, but it significantly increased exosome production in a time-dependent manner. HIF-1 induction with dimethyloxalylglycine also promoted exosome secretion, whereas pharmacological and genetic suppression of HIF-1 abrogated the increase of exosome secretion under hypoxia. The exosomes from hypoxic RPTCs had inhibitory effects on apoptosis of RPTCs following ATP depletion. The protective effects were lost in the exosomes from HIF-1α knockdown cells. It is concluded that hypoxia stimulates exosome production and secretion in renal tubular cells. The exosomes from hypoxic cells are protective against renal tubular cell injury. HIF-1 mediates exosome production during hypoxia and contributes to the cytoprotective effect of the exosomes.

scholarly journals Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0166707 ◽  
Author(s):  
Tadayoshi Konno ◽  
Rei Nakano ◽  
Ryo Mamiya ◽  
Hisashi Tsuchiya ◽  
Taku Kitanaka ◽  
...  
Keyword(s):  
Interleukin 1Β ◽  
Tubular Cells ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
And Function ◽  
Neutrophil Gelatinase

scholarly journals Extracellular Vesicles Released from Mesenchymal Stromal Cells Modulate miRNA in Renal Tubular Cells and Inhibit ATP Depletion Injury

2014 ◽  
Vol 23 (15) ◽  
pp. 1809-1819 ◽  
Author(s):  
Rafael S. Lindoso ◽  
Federica Collino ◽  
Stefania Bruno ◽  
Dayana S. Araujo ◽  
Julliana F. Sant'Anna ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Atp Depletion ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Effects of targeted Bcl-2 expression in mitochondria or endoplasmic reticulum on renal tubular cell apoptosis

2008 ◽  
Vol 294 (3) ◽  
pp. F499-F507 ◽  
Author(s):  
Kirti Bhatt ◽  
Leping Feng ◽  
Navjotsingh Pabla ◽  
Kebin Liu ◽  
Sylvia Smith ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cytochrome C ◽  
Cell Apoptosis ◽  
Atp Depletion ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Wild Type ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Bcl-2 family proteins are central regulators of apoptosis. As the prototypic member, Bcl-2 protects various types of cells against apoptotic insults. In mammalian cells, Bcl-2 has a dual subcellular localization, in mitochondria and endoplasmic reticulum (ER). The respective roles played by mitochondrial and ER-localized Bcl-2 in apoptotic inhibition are unclear. Using Bcl-2 constructs for targeted subcellular expression, we have now determined the contributions of mitochondrial and ER-localized Bcl-2 to the antiapoptotic effects of Bcl-2 in renal tubular cells. Wild-type Bcl-2, when expressed in renal proximal tubular cells, showed partial colocalizations with both cytochrome c and disulfide isomerase, indicating dual localizations of Bcl-2 in mitochondria and ER. In contrast, Bcl-2 constructs with mitochondria-targeting or ER-targeting sequences led to relatively restricted Bcl-2 expression in mitochondria and ER, respectively. Expression of wild-type and mitochondrial Bcl-2 showed significant inhibitory effects on tubular cell apoptosis that was induced by cisplatin or ATP depletion; however, ER-Bcl-2 was much less effective. During ATP depletion, cytochrome c was released from mitochondria into the cytosol. This release was suppressed by wild-type and mitochondrial Bcl-2, but not by ER-Bcl-2. Consistently, wild-type and mitochondrial Bcl-2, but not ER-Bcl-2, blocked Bax activation during ATP depletion, a critical event for mitochondrial outer membrane permeabilization and cytochrome c release. In contrast, ER-Bcl-2 protected against apoptosis during tunicamycin-induced ER stress. Collectively, the results suggest that the cytoprotective effects of Bcl-2 in different renal injury models are largely determined by its subcellular localizations.

Inhibition of apoptosis by Zn2+ in renal tubular cells following ATP depletion

2004 ◽  
Vol 287 (3) ◽  
pp. F492-F500 ◽  
Author(s):  
Qingqing Wei ◽  
Jinzhao Wang ◽  
Mong-Heng Wang ◽  
Fushin Yu ◽  
Zheng Dong
Keyword(s):  
Cytochrome C ◽  
Renal Cell ◽  
Atp Depletion ◽  
Caspase Activation ◽  
Renal Protection ◽  
Cytochrome C Release ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Apoptosis has been implicated in ischemic renal injury. Thus one strategy of renal protection is to antagonize apoptosis. However, apoptosis inhibitory approaches remain to be fully explored. Zn2+ has long been implicated in apoptosis inhibition; but systematic analysis of the inhibitory effects of Zn2+ is lacking. Moreover, whether Zn2+ blocks renal cell apoptosis following ischemia is unknown. Here, we demonstrate that Zn2+ is a potent apoptosis inhibitor in an in vitro model of renal cell ischemia. ATP depletion induced apoptosis in cultured renal tubular cells, which was accompanied by caspase activation. Zn2+ at 10 μM inhibited both apoptosis and caspase activation, whereas Co2+ was without effect. In ATP-depleted cells, Zn2+ partially prevented Bax activation and cytochrome c release from mitochondria. In isolated cell cytosol, Zn2+ blocked cytochrome c-stimulated caspase activation at low-micromolar concentrations. In addition, Zn2+ could directly antagonize the enzymatic activity of purified recombinant caspases. We conclude that Zn2+ is a potent inhibitor of apoptosis in renal tubular cells following ATP depletion. Zn2+ blocks apoptosis at multiple steps including Bax activation, cytochrome c release, apoptosome function, and caspase activation.

scholarly journals Differing regulation and function of ICAM-1 and class II antigens on renal tubular cells

1990 ◽  
Vol 38 (3) ◽  
pp. 417-425 ◽  
Author(s):  
Anthony M. Jevnikar ◽  
Rudolf P. Wuthrich ◽  
Fumio Takei ◽  
Hong-Wu Xu ◽  
Daniel C. Brennan ◽  
...  
Keyword(s):  
Class Ii ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
And Function ◽  
Class Ii Antigens
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