The Biology of Epithelial Cell Tight Junctions in the Kidney

Denker, Bradley M.; Sabath, Ernesto

doi:10.1681/asn.2010090922

Cited by 69 publications

(76 citation statements)

References 32 publications

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“…Tight junction proteins, including cytoplasmic scaffolding proteins, transmembrane proteins, and signaling proteins, act like a biologic zipper, controlling movement of water and solutes in the intercellular passageway (60). Zona occludens protein-1 functions as a scaffold protein, anchoring to other transmembrane proteins and the actin cytoskeleton, helping to seal the intercellular space.…”

Section: Fine-tuning Water Balance In the Collecting Ductmentioning

confidence: 99%

Osmotic Homeostasis

Danziger

Zeidel

2015

Clinical Journal of the American Society of Nephrology

169

103

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Alterations in water homeostasis can disturb cell size and function. Although most cells can internally regulate cell volume in response to osmolar stress, neurons are particularly at risk given a combination of complex cell function and space restriction within the calvarium. Thus, regulating water balance is fundamental to survival. Through specialized neuronal "osmoreceptors" that sense changes in plasma osmolality, vasopressin release and thirst are titrated in order to achieve water balance. Fine-tuning of water absorption occurs along the collecting duct, and depends on unique structural modifications of renal tubular epithelium that confer a wide range of water permeability. In this article, we review the mechanisms that ensure water homeostasis as well as the fundamentals of disorders of water balance.

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Section: Fine-tuning Water Balance In the Collecting Ductmentioning

confidence: 99%

Osmotic Homeostasis

Danziger

Zeidel

2015

Clinical Journal of the American Society of Nephrology

169

103

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“…ZO-1 has been described as the organizer of the TJ because it anchors various components such as occludin and the claudins to the actin cytoskeleton (15,58). Thus it is highly significant that ZO-1 was so strongly disrupted in LPS-induced AKI and may explain the failure of claudin-1, -3, and -4 to increase at the TJ despite an upregulation in transcription for each of them.…”

Section: Discussionmentioning

confidence: 99%

“…ZO-1 is a 220-kDa intracellular scaffolding protein which links membrane-bound components of the TJs to the actin cytoskeleton (17,58). ZO-1 interacts with signaling proteins such as Src as well as the TJ strand composed of claudins and TJ-associated marvel proteins: occludin, tricellulin, and marvelD3 (15,19,38,39,46). The expression of occludin and ZO-1 are higher in the distal nephron than the proximal nephron (21).…”

mentioning

confidence: 99%

Endotoxemia alters tight junction gene and protein expression in the kidney

Eadon

Hack

et al. 2012

American Journal of Physiology-Renal Physiology

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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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“…However, we found no changes in the protein level. These discrepant results may be related to the fact that ZO-1 is located exclusively at the TJ and links TJ proteins to each other [6]. Whether ZO-1 has a role in paracellular NaCl transport in the kidney needs to be answered in the future.…”

Section: Discussionmentioning

confidence: 99%

“…Paracellular NaCl transport through the tight junction (TJ) occurs along the nephron, and the TJ includes integral membrane proteins such as claudins and occludin, scaffolding proteins such as zonula occludens-1 (ZO-1), and signaling proteins from all major families of G proteins, kinases, and phosphatases [6]. In addition to active sodium transport, passive diffusion of NaCl through paracellular pathways contributes to renal interstitial hydrostatic pressure (RIHP) and may affect pressure natriuresis [7].…”

Section: Introductionmentioning

confidence: 99%

Alteration of Tight Junction Protein Expression in Dahl Salt-Sensitive Rat Kidney

Kim

et al. 2017

Kidney Blood Press Res

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Background/Aims: Altered pressure natriuresis is an important mechanism of hypertension, but it remains elusive at the molecular level. We hypothesized that in the kidney, tight junctions (TJs) may have a role in pressure natriuresis because paracellular NaCl transport affects interstitial hydrostatic pressure. Methods: To assess the association of salt-sensitive hypertension with altered renal TJ protein expression, Dahl salt-sensitive (SS) and salt-resistant (SR) rats were put on an 8% NaCl-containing rodent diet for 4 weeks. Systolic blood pressure (SBP) and urine NaCl excretion were measured weekly, and kidneys were harvested for immunoblotting and quantitative PCR analysis at the end of the animal experiments. Results: SBP was significantly higher in SS rats than in SR rats during the first to fourth weeks of the animal experiments. During the first and second week, urinary NaCl excretion was significantly lower in SS rats as compared with SR rats. However, the difference between the two groups vanished at the third and fourth weeks. In the kidney, claudin-4 protein and mRNA were significantly increased in SS rats as compared with SR rats. On the other hand, occludin protein and mRNA were significantly decreased in SS rats as compared with SR rats. The expression of claudin-2, claudin-7, and claudin-8 did not vary significantly between the two groups. Conclusions: In SS rats, SS hypertension was associated with differential changes in renal TJ protein expression. Both upregulation of claudin-4 and downregulation of occludin might increase paracellular NaCl transport in the kidney, resulting in impaired pressure natriuresis in SS rats.

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The Biology of Epithelial Cell Tight Junctions in the Kidney

Cited by 69 publications

References 32 publications

Osmotic Homeostasis

Osmotic Homeostasis

Endotoxemia alters tight junction gene and protein expression in the kidney

Alteration of Tight Junction Protein Expression in Dahl Salt-Sensitive Rat Kidney

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