Bcl-2 and Bax expression on rat ischemic kidney

Eschwège, P.; Paradis, Valérie; Conti, Marc; Loric, Sylvain; Dumas, Frédéric; Berteau, Pierre; Ahmed, Md. Kawser; Droupy, S.; Charpentier, B; Legrand, Alain; Bédossa, Pierre; Galand, Benoît

doi:10.1016/s0041-1345(98)00844-6

Cited by 5 publications

(3 citation statements)

References 4 publications

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“…The signal of N-cadherin was abolished by renal artery clamping. There was no change following ischemia in BCL-2 for comparison, as previously reported (Eschwege et al 1998) ischemia has been shown to induce loss of surface membrane polarity (Molitoris 2004). Our data further support the hypothesis that disruption of adherens junctions contributes to the loss of epithelial polarity observed in AKI.…”

Section: Discussionsupporting

confidence: 90%

N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury

Nürnberger

Feldkamp

Kavapurackal

et al. 2010

Histochem Cell Biol

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Ischemia remains the most common cause of acute kidney injury (AKI). Decreased intercellular adhesion and alterations in adhesion molecules may contribute to the loss of renal function observed in AKI. In the present study, we evaluated the distribution of adhesion molecules in the human kidney and analyzed their expression in human and experimental AKI. Specimens of human kidneys obtained from patients with and without AKI were stained for the cell adhesion molecules E-cadherin, N-cadherin and beta-catenin. Experimental AKI in rats was induced by renal artery clamping. Immunostaining and immunoblotting were carried out for E-cadherin, N-cadherin and beta-catenin. Proximal tubule cells from opossum kidneys (OKs) were used to analyze the effect of chemical hypoxia (ATP depletion) in vitro. In the adult human kidney, N-cadherin was expressed in proximal tubules, while E-cadherin was expressed in other nephron segments. beta-Catenin was expressed in both proximal and distal tubules. In human AKI and in ischemic rat kidneys, N-cadherin immunostaining was depleted from proximal tubules. There was no change in E-cadherin or beta-catenin. In vitro, OK cells expressed N-cadherin only in the presence of collagen, and ATP depletion led to a depletion of N-cadherin. Collagen IV staining was reduced in ischemic rat kidneys compared to controls. The results of the study suggest that N-cadherin may play a significant role in human and experimental AKI.

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Section: Discussionsupporting

confidence: 90%

N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury

Nürnberger

Feldkamp

Kavapurackal

et al. 2010

Histochem Cell Biol

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“…Despite extensive studies in either field, there is only limited information on the role of Bcl-2 and Bax in CKD. In vivo, Bcl-2 and Bax proteins have not been detected in the kidneys during ischemia (28), whereas the overexpression of Bcl-2 can suppress the apoptosis of renal tubule cells induced by hypoxia/reoxygenation (29). Moreover, an increase in the Bax/Bcl-2 ratio by hypoxia/reoxygenation or ischemia/reperfusion injury triggers Bax translocation to the mitochondria and cytochrome c release to cytoplasm, and enhances caspase-3-mediated renal tubular apoptosis (30).…”

Section: Discussionmentioning

confidence: 97%

Berberine prevents the apoptosis of mouse podocytes induced by TRAF5 overexpression by suppressing NF-κB activation

Yao

Lan

et al. 2017

Int J Mol Med

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Berberine (BBR) has previously been found to exert beneficial effects on renal injury in experimental rats. However, the mechanisms underlying these effects are not yet fully understood. Tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) has been demonstrated to mediate the activation of nuclear factor-κB (NF-κB), which has been implicated in the pathogenesis of chronic kidney disease (CKD). The aim of this study was to investigate the effects of BBR on kidney injury and the activation of the NF-κB signaling pathway in mouse podocytes. TRAF5 was found to be overexpressed in patients with CKD and chronic renal failure (CRF) (data obtained from the dataset GSE48944, as well as from patients at Shuguang Hospital). TRAF5 overexpression significantly inhibited cell viability and induced the apoptosis of mouse podocytes. However, BBR prevented the decrease in cell viability and the apoptosis induced by TRAF5 overexpression. The NF-κB inhibitor, caffeic acid phenethyl ester (CAPE), mimicked the protective effects of BBR, as evidenced by the increased expression of nephrin and podocin, and the decreased the expression of caspase-3 and the ratio of Bax/Bcl-2. Moreover, BBR prevented the decrease in cell viability decrease and the apoptosis induced by TNF-α, interleukin (IL)-6 and lipopolysaccharide (LPS). Taken together, our data indicate that BBR exerts protective effects against CRF partly through the TRAF5-mediated activation of the NF-κB signaling pathway in mouse podocytes.

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“…Previous studies examining bcl-2 expression during renal I/R injury are conflicting. Bcl-2 expression was either not detected by immunohistochemistry during I/R [39] or was present in the damaged (apoptotic) distal tubules [40]. Other studies found that regenerating proximal tubules express elevated bcl-2 mRNA after renal injury suggesting its role in repair of the damaged proximal tubule after ischemia [41].…”

Section: Discussionmentioning

confidence: 99%

CREB mediates ERK-induced survival of mouse renal tubular cells after oxidant stress

Arany

Megyesi

Reusch

et al. 2005

Kidney International

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Bcl-2 and Bax expression on rat ischemic kidney

Cited by 5 publications

References 4 publications

N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury

N-cadherin is depleted from proximal tubules in experimental and human acute kidney injury

Berberine prevents the apoptosis of mouse podocytes induced by TRAF5 overexpression by suppressing NF-κB activation

CREB mediates ERK-induced survival of mouse renal tubular cells after oxidant stress

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