Neonatal Hyperoxia Downregulates Claudin-4, Occludin, and ZO-1 Expression in Rat Kidney Accompanied by Impaired Proximal Tubular Development

Xu, Xuewen; Zhang, Xinyue; Gao, Linlin; Liu, Chunfeng; You, Kai

doi:10.1155/2020/2641461

Cited by 13 publications

(8 citation statements)

References 55 publications

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“…Tubular damage rate, which is one of the histopathological findings of the hyperoxia effect in our study (Figs. 1, 2 and 3), was also shown in some studies in the literature [2,[27][28][29] in neonatal rat kidneys, but unlike these studies, we preferred adult rats in our study. Xu et al stated that inhibited expression of tight junction proteins (claudin-4, occludin, and ZO-1) in proximal tubules might be a potential mechanism of neonatal hyperoxia-induced nephrogenic disorders [28].…”

Section: Discussionmentioning

confidence: 74%

“…1, 2 and 3), was also shown in some studies in the literature [2,[27][28][29] in neonatal rat kidneys, but unlike these studies, we preferred adult rats in our study. Xu et al stated that inhibited expression of tight junction proteins (claudin-4, occludin, and ZO-1) in proximal tubules might be a potential mechanism of neonatal hyperoxia-induced nephrogenic disorders [28]. In the analysis of the histopathological findings of our study, we see that the state of hyperoxia causes glomerular and tubular damage due to increased oxidative stress, and this damage rate does not improve much with the use of tadalafil (Tables 2 and 3).…”

Section: Discussionmentioning

confidence: 74%

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The danger of hyperoxia on the rat kidneys: is tadalafil a real shield?

et al. 2022

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Purpose Continuous oxygen therapy to compensate for decreased oxygen saturation in the blood is a life-saving treatment used in case lung involvement. Excess oxygen delivery was reported to be a common situation, in which about 50% of the patients showed hyperoxemia and 4% in severe hyperoxemia. In this work, we investigated the effects of hyperoxia on the rat kidneys and whether tadalafil has an effect to reduce this damage. Materials and methods Three groups of 8 male rats each weighing 300–350 g were formed. The groups were divided into the control group, hyperoxia group, and hyperoxia and tadalafil administered group for 10 days. At the end of the 10th day, blood and kidney samples were taken for biochemical analysis (SOD and NO levels) and histopathological examination. Results While our findings showed that SOD levels were significantly different among the control and experimental groups and within the experimental groups, no statistical difference was found in terms of NO levels among the groups (Table 1). While the glomerular and tubular injury was higher in the Hyperoxia group and the Hyperoxia + Tadalafil group than in the control group ( p < 0.001), as a result of the rate of severe glomerular and tubular injury in the hyperoxia group, was 62.5% and 43.8% and in the group given tadalafil was 43.8% and 31.3%, respectively (Table 2). Conclusions Exposure to hyperoxia condition causes renal glomerular and tubular damage, and tadalafil does not show a protective effect on this damage according to this study’s dose and exposure time.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 74%

The danger of hyperoxia on the rat kidneys: is tadalafil a real shield?

et al. 2022

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“…44 An additional study suggested that the mechanism of hyperoxic nephropathy may be related to impaired tight junction proteins in the kidney, and that neonatal hyperoxia extensively inhibits the expression of tight junction proteins during proximal tubule development, possibly by downregulating proximal tubule claudin-4 expression and perhaps mediated through IL-6 and TNF-α; however, the inhibition of expression mediated by IL-6 and TNF-α are only involved in hyperoxia-induced renal damage and are not dependent on their proinflammatory effects. 45 Moreover, a mouse model study found no change in the number of kidney units in mice exposed to 65% oxygen 18 and no significant long-term deleterious effects on glomerular structure. Conversely, early exposure to 80% oxygen resulted in hypertension, changes in vascular function, and reduced kidney unit function in adulthood.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

The Mechanism of Hyperoxia-Induced Neonatal Renal Injury and the Possible Protective Effect of Resveratrol

2022

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With recent advances in neonatal intensive care, preterm infants are surviving into adulthood. Nonetheless,epidemiological data on the health status of these preterm infants has begun to reveal a worrying theme; prematurity and the supplemental oxygen therapy these infants receive after birth appear to be risk factors for kidney disease in in adulthood, affecting their quality-of-life. As the incidence of chronic kidney disease and the survival time of preterm infants both increase, the management of hyperoxia-induced renal disease is becoming increasingly relevant to neonatologists. The mechanism of this increased risk is currently unknown, but prematurity itself and the hyperoxia exposure after birth may predispose to disease by altering the normal trajectory of kidney maturation. This article reviews altered renal reactivity due to hyperoxia, the possible mechanisms of renal injury due to hyperoxia, and the role of resveratrol in renal injury.

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“…Although prior work has focused primarily on the role of ZO-1 in slit diaphragm, it has been demonstrated that ZO-1 is also abundantly expressed in renal tubule epithelial cells [108,119,120]. The ZO-1/ZONAB signal pathway is indispensable for modulating epithelial phenotype.…”

Section: Zo-1mentioning

confidence: 99%

Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease

Sun

Liu

2022

IJMS

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Matrix metalloproteinase-10 (MMP-10) is a zinc-dependent endopeptidase with the ability to degrade a broad spectrum of extracellular matrices and other protein substrates. The expression of MMP-10 is induced in acute kidney injury (AKI) and chronic kidney disease (CKD), as well as in renal cell carcinoma (RCC). During the different stages of kidney injury, MMP-10 may exert distinct functions by cleaving various bioactive substrates including heparin-binding epidermal growth factor (HB-EGF), zonula occludens-1 (ZO-1), and pro-MMP-1, -7, -8, -9, -10, -13. Functionally, MMP-10 is reno-protective in AKI by promoting HB-EGF-mediated tubular repair and regeneration, whereas it aggravates podocyte dysfunction and proteinuria by disrupting glomerular filtration integrity via degrading ZO-1. MMP-10 is also involved in cancerous invasion and emerges as a promising therapeutic target in patients with RCC. As a secreted protein, MMP-10 could be detected in the circulation and presents an inverse correlation with renal function. Due to the structural similarities between MMP-10 and the other MMPs, development of specific inhibitors targeting MMP-10 is challenging. In this review, we summarize our current understanding of the role of MMP-10 in kidney diseases and discuss the potential mechanisms of its actions.

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Neonatal Hyperoxia Downregulates Claudin-4, Occludin, and ZO-1 Expression in Rat Kidney Accompanied by Impaired Proximal Tubular Development

Cited by 13 publications

References 55 publications

The danger of hyperoxia on the rat kidneys: is tadalafil a real shield?

The danger of hyperoxia on the rat kidneys: is tadalafil a real shield?

The Mechanism of Hyperoxia-Induced Neonatal Renal Injury and the Possible Protective Effect of Resveratrol

Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease

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