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Renal Tubular Epithelial Cells (renal + tubular_epithelial_cell)
Selected AbstractsIncreasing Resistance of Tubular Epithelial Cells to Apoptosis by shRNA Therapy Ameliorates Renal Ischemia-Reperfusion InjuryAMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2006C. Du Renal tubular epithelial cells (TEC) die by apoptosis or necrosis in renal ischemia-reperfusion injury (IRI). Fas/Fas ligand-dependent fratricide is critical in TEC apoptosis, and Fas promotes renal IRI. Therefore, targeting Fas or caspase-8 may have therapeutic potential for renal injury in kidney transplant or failure. RNA silencing by short hairpin RNA (shRNA) is a novel strategy to down-regulate protein expression. Using this approach, silencing of Fas or caspase-8 by shRNA to prevent TEC apoptosis and IRI was evaluated. IRI was induced by renal artery clamping for 45 or 60 min at 32°C in uninephrectomized C57BL/6 mice. Here, we showed that Fas or pro-caspase-8 expression was significantly knocked down in TEC by stable expression of shRNA, resulting in resistance to apoptosis induced by superoxide, IFN-,/TNF-, and anti-Fas antibody. Inferior vena cava delivery of pHEX-small interfering RNA targeting Fas or pro-caspase-8 resulted in protection of kidney from IRI, indicated by reduction of renal tubular injury (necrosis and apoptosis) and serum creatinine or blood urea nitrogen. Our data suggest that shRNA-based therapy targeting Fas and caspase-8 in renal cells can lead to protection of kidney from IRI. Attenuation of pro-apoptotic proteins using genetic manipulation strategies such as shRNA might represent a novel strategy to promote kidney allograft survival from rejection or failure. [source] Edwardsiella tarda infection in Korean catfish, Silurus asotus, in a Korean fish farmAQUACULTURE RESEARCH, Issue 1 2009Jin-Ha Yu Abstract Mass mortality of Korean catfish, Silurus asotus, occurred in a culture farm situated in Jeollabukdo Province, Korea. The cumulative mortality rates reached up to 5% of the total fish in the farm per day. In clinical signs, the affected fish showed abdominal distension, vent protrusion, enteritis, liver congestion and abscess-like lesions in enlarged spleen and kidney. Histopathologically, in the liver, hepatocytes lost fat and underwent atrophy or necrosis. The spleen showed necrotized splenocytes and a haemorrhagic pulp. In the kidney, glomerular destruction, degeneration of renal tubular epithelial cell and haemorrhage were observed. However, necrotic muscular lesions were not observed. A pure bacterial isolate was obtained from the liver, spleen and kidney lesions of affected fish. Experimental infection of normal catfish with the isolate resulted in the development of clinical signs similar to those seen on the farm. The isolates were identified as Edwardsiella tarda through biochemical tests (99.4%) and analysis of bacterial genes (16S rDNA) sequences (98%). The bacteria possessed two virulent genes: sodB and katB genes. These results suggest that E. tarda can act as a pathogen of farmed catfish. This is the first report showing that E. tarda caused mortality in cultured Korean catfish. [source] Mechanism of calcium oxalate renal stone formation and renal tubular cell injuryINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2008Masao Tsujihata Abstract: Formation of calcium oxalate stones tends to increase with age and begins from the attachment of a crystal formed in the cavity of renal tubules to the surface of renal tubular epithelial cells. Though most of the crystals formed in the cavity of renal tubules are discharged as is in the urine, in healthy people, crystals that attach to the surface of renal tubular epithelial cells are thought to be digested by macrophages and/or lysosomes inside of cells. However, in individuals with hyperoxaluria or crystal urine, renal tubular cells are injured and crystals easily become attached to them. Various factors are thought to be involved in renal tubular cell injury. Crystals attached to the surface of renal tubular cells are taken into the cells (crystal,cell interaction). And then the crystal and crystal aggregates grow, and finally a stone is formed. [source] Paradoxical enhancement of oxidative cell injury by overexpression of heme oxygenase-1 in an anchorage-dependent cell ECV304JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2004Keiko Maruhashi Abstract There has been increasing evidence suggesting the potent anti-inflammatory roles of heme oxygenase-1 (HO-1) in protecting renal tubular epithelial cells, vascular endothelial cells, and circulating monocytes. Based on these findings, novel therapeutic interventions have been proposed to control the expression of endothelial HO-1 levels to ameliorate various vascular diseases. We evaluated the effect of HO-1 gene transfer into an anchorage-dependent cell, ECV304. Effect of HO-1 production on the cell injury induced by hydrogen peroxide was evaluated after hemin stimulation and after HO-1 gene transfection. Morphological changes and the induction of various anti-apoptotic proteins were examined at the same time. Levels of HO-1 expression were variable in different clones of HO-1-transfected ECV304 cells. Among these, the clones with moderate levels of HO-1 expression were significantly more resistant to oxidative stress. In contrast, those with the highest levels of HO-1 exhibited paradoxically enhanced susceptibility to oxidative injury. Interestingly, the cell survival after oxidative stress was in parallel with the levels of Bcl-2 expression and of fibronectin receptor, ,5 integrin. It is suggested from these results, that excessive HO-1 not only leads to enhanced cell injury, but also prolongs the repair process of the injured endothelial tissue. However, HO-1 reduces the oxidative cell injury and protects the endothelial cells, if its expression is appropriately controlled. © 2004 Wiley-Liss, Inc. [source] | ||||||||||