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Renal ischemia–reperfusion injury causes intercalated cell-specific disruption of occludin in the collecting duct

التفاصيل البيبلوغرافية
العنوان: Renal ischemia–reperfusion injury causes intercalated cell-specific disruption of occludin in the collecting duct
المؤلفون: H. Moo Kwon, Su Youn Lee, Ki Hwan Han, Jung A. Shin, I. David Weiner
المصدر: Histochemistry and Cell Biology
بيانات النشر: Springer-Verlag, 2011.
سنة النشر: 2011
مصطلحات موضوعية: Collecting duct, Male, medicine.medical_specialty, Histology, Blotting, Western, Ischemia/reperfusion injury, 030204 cardiovascular system & hematology, Biology, Occludin, Kidney, Models, Biological, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Loop of Henle, Animals, Intercalated Cell, Distal convoluted tubule, Molecular Biology, Tight junction, 030304 developmental biology, Epithelial polarity, 0303 health sciences, Original Paper, urogenital system, Membrane Proteins, Cell Biology, Acidosis, Renal Tubular, Phosphoproteins, Immunohistochemistry, Cell biology, Rats, Medical Laboratory Technology, Endocrinology, Tubule, medicine.anatomical_structure, Kidney Tubules, Reperfusion Injury, Zonula Occludens-1 Protein
الوصف: Renal ischemic events open tight junctions and disrupt epithelial polarity. The purpose of this study was to examine the effects of ischemia-reperfusion (IR) injury on expression and distribution of the tight junction proteins, occludin and ZO-1, in the rat kidney. IR injury was induced by clamping both renal pedicles for 30 min and animals were killed at 6 h after the reperfusion. IR injury decreased blood bicarbonate level, but did not persistently alter pH, Na(+), K(+), or Cl(-). In control kidneys, occludin immunoreactivity was intense in the tight junctions in the thick ascending limb, distal convoluted tubule, and collecting duct, moderate in the thin limbs of the loop of Henle, and was not detected in the proximal tubule, glomerulus, and blood vessels. ZO-1 was expressed in the same sites in which occludin was expressed, and additionally was also expressed in the proximal tubule, glomerulus, and vascular endothelial cells. IR kidneys exhibited damaged renal tubular epithelial cells in both proximal tubule and collecting duct segments in the outer medulla. In the collecting duct, the response of intercalated cells and principal cells differed. Following IR injury, intercalated cells, but not principal cells, lost their normal epithelial polarity and were frequently extruded into the tubule lumen. Occludin, instead of being localized to tight junctions, was localized diffusely in the cytoplasm in intercalated cells of IR kidneys. Principal cells, in contrast, were not detectably affected and neither occludin nor ZO-1 expression were altered in response to IR injury. The normal localization of ZO-1 expression to tight junction sites in both the proximal tubule and collecting duct was altered in response to IR, and, instead, ZO-1 expression was present diffusely in the cytoplasm. IR injury did not alter detectably either occludin or ZO-1 localization to the tight junction of the thick ascending limb cells. The abundance of total occludin protein by immunoblot analysis was not changed with IR injury. These results demonstrate that renal IR injury causes tight junction disruptions in both the proximal tubule and the collecting duct, and that altered distribution of the tight junction protein, occludin, may play a critical role in the collecting duct dysfunction which IR induces.
اللغة: English
تدمد: 1432-119X
0948-6143
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::352fcb2ebb7a5a4475021d86194e1701
http://europepmc.org/articles/PMC3214267
Rights: OPEN
رقم الانضمام: edsair.doi.dedup.....352fcb2ebb7a5a4475021d86194e1701
قاعدة البيانات: OpenAIRE
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