Ultrastructure of Tubular Epithelial Cells in Response to Microembolism-Induced Chronic Ischemic Injury in Rats

2004 ◽  
Vol 95 (4) ◽  
pp. e144-e151 ◽  
Author(s):  
Yoshihide Fujigaki ◽  
Masato Kimura ◽  
Mitsuko Asano ◽  
Takayuki Suzuki ◽  
Akira Hishida
Keyword(s):  
Epithelial Cells ◽  
Ischemic Injury ◽  
Tubular Epithelial Cells

scholarly journals JAK2/Y343/STAT5 signaling axis is required for erythropoietin-mediated protection against ischemic injury in primary renal tubular epithelial cells

2008 ◽  
Vol 295 (6) ◽  
pp. F1689-F1695 ◽  
Author(s):  
A. C. Breggia ◽  
D. M. Wojchowski ◽  
J. Himmelfarb
Keyword(s):  
Epithelial Cells ◽  
Tissue Injury ◽  
Ischemic Injury ◽  
Erythropoietin Receptor ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Primary Mouse ◽  
Signaling Axis ◽  
Renal Tubular

Erythropoietin has emerged as a potential therapy for the treatment of ischemic tissue injury. In erythroid cells, the JAK2/Y343/STAT5 signaling axis has been shown to be necessary for stress but not steady-state erythropoiesis. The requirement for STAT5 activation in erythropoietin-mediated protection from ischemic injury has not been well-studied. To answer this question, we induced reproducible necrotic ischemic injury in primary mouse renal tubular epithelial cells (RTEC) in vitro. Using RTEC from erythropoietin receptor mutant mice with differential STAT5 signaling capabilities, we demonstrated first, that EPO administration either before or during injury significantly protects against mild-moderate but not severe necrotic cell death; and second, the JAK2/Y343/STAT5 signaling axis is required for protection against ischemic injury in primary mouse RTEC. In addition, we identified Pim-3, a prosurvival STAT5 target gene, as responsive to EPO in the noninjured kidney both in vitro and in vivo.

scholarly journals Increased susceptibility of aging kidney to ischemic injury: identification of candidate genes changed during aging, but corrected by caloric restriction

2007 ◽  
Vol 293 (4) ◽  
pp. F1272-F1281 ◽  
Author(s):  
G. Chen ◽  
E. A. Bridenbaugh ◽  
A. D. Akintola ◽  
J. M. Catania ◽  
V. S. Vaidya ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Candidate Genes ◽  
Caloric Restriction ◽  
Molecular Mechanism ◽  
Ischemic Injury ◽  
Histological Evaluation ◽  
Tubular Epithelial Cells ◽  
Increased Susceptibility

Aging is associated with an increased incidence and severity of acute renal failure. However, the molecular mechanism underlying the increased susceptibility to injury remains undefined. These experiments were designed to investigate the influence of age on the response of the kidney to ischemic injury and to identify candidate genes that may mediate this response. Renal slices prepared from young (5 mo), aged ad libitum (aged-AL; 24 mo), and aged caloric-restricted (aged-CR; 24 mo) male Fischer 344 rats were subjected to ischemic stress (100% N2) for 0–60 min. As assessed by biochemical and histological evaluation, slices from aged-AL rats were more susceptible to injury than young counterparts. Importantly, caloric restriction attenuated the increased susceptibility to injury. In an attempt to identify the molecular pathway(s) underlying this response, microarray analysis was performed on tissue harvested from the same animals used for the viability experiments. RNA was isolated and the corresponding cDNA was hybridized to CodeLink Rat Whole Genome Bioarray slides. Subsequent gene expression analysis was performed using GeneSpring software. Using two-sample t-tests and a twofold cut-off, the expression of 92 genes was changed during aging and attenuated by caloric restriction, including claudin-7, kidney injury molecule-1 (Kim-1), and matrix metalloproteinase-7 (MMP-7). Claudin-7 gene expression peaked at 18 mo; however, increased protein expression in certain tubular epithelial cells was seen at 24 mo. Kim-1 gene expression was not elevated at 8 or 12 mo but was at 18 and 24 mo. However, changes in Kim-1 protein expression were only seen at 24 mo and corresponded to increased urinary levels. Importantly, these changes were attenuated by caloric restriction. MMP-7 gene expression was decreased at 8 mo, but an age-dependent increase was seen at 24 mo. Increased MMP-7 protein expression in tubular epithelial cells at 24 mo was correlated with the gene expression pattern. In summary, we identified genes changed by aging and changes attenuated by caloric restriction. This will facilitate investigation into the molecular mechanism mediating the age-related increase in susceptibility to injury.

scholarly journals Binding of factor H to tubular epithelial cells limits interstitial complement activation in ischemic injury

2011 ◽  
Vol 80 (2) ◽  
pp. 165-173 ◽  
Author(s):  
Brandon Renner ◽  
Viviana P. Ferreira ◽  
Claudio Cortes ◽  
Ryan Goldberg ◽  
Danica Ljubanovic ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Complement Activation ◽  
Ischemic Injury ◽  
Factor H ◽  
Tubular Epithelial Cells

scholarly journals Primary Mouse Renal Tubular Epithelial Cells Have Variable Injury Tolerance to Ischemic and Chemical Mediators of Oxidative Stress

2008 ◽  
Vol 1 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Anne C. Breggia ◽  
Jonathan Himmelfarb
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Ischemic Injury ◽  
Culture Method ◽  
Antimycin A ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Primary Mouse ◽  
Ldh Release ◽  
Renal Tubular

We have developed and evaluated an in vitro culture method for assessing ischemic injury in primary mouse renal tubular epithelial cells (RTEC) in which to explore the pathobiology underlying acute kidney injury. RTEC were predominately of proximal tubule origin which is most susceptible to ischemic injury as compared to other nephron segments. Oxidative stress was induced by chemically depleting ATP using Antimycin A and 2-Deoxy-D-Glucose and by exposing cells to a 1% oxygen environment. Necrotic injury was assessed by measuring LDH released into culture supernatants. Optimal dose and time of exposure to each injury agent was determined for induction of mild, moderate and severe ischemic injury defined as LDH release of ≤20%, 21–49% and ≥50% above baseline respectively. Antimycin A and 2-Deoxy-D-Glucose produced a progressive increase in LDH release which was time dependent but chemical concentration independent. A 1% oxygen environment also induced cell injury over time but only if glucose was absent from the culture media. Antimycin A was most effective at inducing oxidative stress causing a mean LDH release of 61% at 48 hr compared to 19% and 50% LDH release induced by 2-Deoxy-D-Glucose and by exposure to 1% oxygen respectively at the same 48 hour time point.The cell culture method described provides several advantages including the use of serum free media and the ability to grow primary cells without matrix support. The LDH assay for injury assessment is reproducible, cost effective, objective and minimizes background cell death. A simple method for the culture and injury of primary mouse renal tubular epithelial cells has thereby been established and provides a useful tool for future investigations of ischemic kidney injury.

Intranuclear Crystals in Regenerating Canine Kidneys

1973 ◽  
Vol 31 ◽  
pp. 412-413
Author(s):  
D.G. Osborne ◽  
L.J. McCormack ◽  
M.O. Magnusson ◽  
W.S. Kiser
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Tubular Epithelial Cell ◽  
Tubular Epithelial Cells ◽  
Cell Nuclei ◽  
Crystalline Structures ◽  
Small Crystals ◽  
Membrane Bound

During a project in which regenerative changes were studied in autotransplanted canine kidneys, intranuclear crystals were seen in a small number of tubular epithelial cells. These crystalline structures were seen in the control specimens and also in regenerating specimens; the main differences being in size and number of them. The control specimens showed a few tubular epithelial cell nuclei almost completely occupied by large crystals that were not membrane bound. Subsequent follow-up biopsies of the same kidneys contained similar intranuclear crystals but of a much smaller size. Some of these nuclei contained several small crystals. The small crystals occurred at one week following transplantation and were seen even four weeks following transplantation. As time passed, the small crystals appeared to fuse to form larger crystals.

miR-877-3p Induces Apoptosis by Targeting BCL2 in Tubular Epithelial Cells

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 506-P
Author(s):  
MEINA ZOU ◽  
MENG XUE ◽  
FANG HU ◽  
YIJIE JIA ◽  
YAN-LIN YANG ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tubular Epithelial Cells
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