ArticleAmerican journal of physiology. Renal physiology2012
Endotoxemia alters tight junction gene and protein expression in the kidney.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Changes in the Tissue Barrier after Exposure to Lipopolysaccharide on the Apical Side of Enterocytes and the Follicle-Associated Epithelium in Peyer's Patches of the Rat Intestine.Bulletin of experimental biology and medicine · 2024Article
- ZFYVE21 promotes endothelial nitric oxide signaling and vascular barrier function in the kidney during aging.Kidney international · 2024Article
- Involvement of Gut Microbiota in SLE and Lupus Nephritis.Biomedicines · 2023Review
- PAI-1 as a critical factor in the resolution of sepsis and acute kidney injury in old age.Frontiers in cell and developmental biology · 2023Article
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- Roxadustat (FG-4592) Facilitates Recovery From Renal Damage by Ameliorating Mitochondrial Dysfunction Induced by Folic Acid.Frontiers in pharmacology · 2021Article
- Septic acute kidney injury: a review of basic research.Clinical and experimental nephrology · 2020Review
- Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture.Experimental and therapeutic medicine · 2020Article
- Functional roles of Grainyhead-like transcription factors in renal development and disease.Pediatric nephrology (Berlin, Germany) · 2020Review
- Toll-Like Receptor-Mediated Cardiac Injury during Experimental Sepsis.Mediators of inflammation · 2020Article
- Deregulated renal magnesium transport during lipopolysaccharide-induced acute kidney injury in mice.Pflugers Archiv : European journal of physiology · 2019Article
- [Expression and significance of tight junction proteins in the kidney in a mouse model of renal ischemia-reperfusion injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018Article
- Lipopolysaccharide Mediates the Destruction of Intercellular Tight Junction among Renal Tubular Epithelial Cells via RhoT1/SMAD-4/JAM-3 Pathway.International journal of medical sciences · 2018Article
- Development of a zebrafish sepsis model for high-throughput drug discovery.Molecular medicine (Cambridge, Mass.) · 2017Article
- Article
- Peroxisomes and Kidney Injury.Antioxidants & redox signaling · 2016Review
- The effect of omega- 3 polyunsaturated fatty acids on endothelial tight junction occludin expression in rat aorta during lipopolysaccharide-induced inflammation.Iranian journal of basic medical sciences · 2016Article
- TNF ROCKs the boat as the kidney endothelium springs a leak.Physiological reports · 2016Article
- Article
- TNF causes changes in glomerular endothelial permeability and morphology through a Rho and myosin light chain kinase-dependent mechanism.Physiological reports · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intact tight junctional (TJ) proteins are required for tubular ion transport and waste excretion. Disruption of TJs may contribute to a decreased glomerular filtration rate in acute kidney injury (AKI) via tubular backleak. The effect of LPS-mediated AKI on murine TJs has not been studied extensively. We hypothesized LPS endotoxin administration to mice would disrupt tubular TJ proteins including zonula occludens-1 (ZO-1), occludin, and claudins. ZO-1 and occludin immunofluorescence 24 h post-LPS revealed a marked change in localization from the usual circumferential fencework pattern to one with substantial fragmentation. Renal ZO-1 expression was significantly reduced 24 h after LPS (decrease of 56.1 ± 7.4%, P < 0.001), with subsequent recovery. ZO-1 mRNA expression was increased 24 h post-LPS (4.34 ± 0.87-fold, P = 0.0019), suggesting disruption of ZO-1 protein is not mediated by transcriptional regulation, but rather by degradation or changes in translation. Similarly, claudin-4 protein expression was decreased despite elevated mRNA. LPS administration resulted in dephosphorylation of occludin and fragmented tubular redistribution. Protein expression of claudin-1, and -3 was increased after LPS. ZO-1, occludin, and claudin-1, -3, and -4 gene expression were increased 48 h after LPS, suggesting a renal response to strengthen TJs following injury. Interestingly, reduced mRNA expression was found only for claudin-8. This study provides further support that LPS-induced AKI is associated with structural injury and is not merely due to hemodynamic changes.
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