Regulation of renal tubular cell apoptosis and proliferation after ischemic injury to a solitary kidney

Oberbauer, Rainer; Schwarz, Christoph; Regele, Heinz; Hansmann, Cornelia; Meyer, Timothy W.; Mayer, Gert

doi:10.1067/mlc.2001.118926

Cited by 34 publications

(25 citation statements)

References 25 publications

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“…found in experimental models of acute renal failure (33). In contrast, Bcl-2 expression is reported to be down-regulated after ischemic renal damage (34).…”

Section: Discussionmentioning

confidence: 96%

Involvement of Peripheral Benzodiazepine Receptor in the Oxidative Stress, Death-Signaling Pathways, and Renal Injury Induced by Ischemia-Reperfusion

Kunduzova

Escourrou²,

Salvayre³

et al. 2004

Journal of the American Society of Nephrology

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The peripheral benzodiazepine receptor (PBR) is a critical component of the mitochondrial permeability transition pore, which is involved in the regulation of cell death. In the present study we investigated the role of PBR in the regulation of signaling pathways leading to apoptotic and necrotic damage and renal dysfunction in a rat model of ischemia-reperfusion. Renal ischemia-reperfusion led to extended tubular apoptosis and necrosis that were associated with peroxidative damage, high levels of proapoptotic Bax expression, and low levels of antiapoptotic Bcl-2 expression, cleavage of death substrate, poly(ADP-ribose) polymerase (PARP), and activation of a key effector of apoptosis, caspase-3. Rat pretreatment with a novel PBR antagonist, SSR180575, significantly decreased postreperfusion oxidative stress and tubular apoptosis and necrosis. This effect was associated with inhibition of caspase-3 activation and PARP cleavage, upregulation of Bcl-2, and downregulation of Bax. Furthermore, inhibition of PBR accelerated the recovery of normal renal function, as assessed by measurement of levels of plasma creatinine and blood urea nitrogen. These findings reveal a role for PBR as a modulator of necrotic and apoptotic cell death induced by ischemia-reperfusion and suggest that regulation of PBR may provide new therapeutic implications for the prevention of acute renal failure.

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“…found in experimental models of acute renal failure (33). In contrast, Bcl-2 expression is reported to be down-regulated after ischemic renal damage (34).…”

Section: Discussionmentioning

confidence: 96%

Involvement of Peripheral Benzodiazepine Receptor in the Oxidative Stress, Death-Signaling Pathways, and Renal Injury Induced by Ischemia-Reperfusion

Kunduzova

Escourrou²,

Salvayre³

et al. 2004

Journal of the American Society of Nephrology

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“…Distal tubular epithelial cells are more resistant to IR injury via antiapoptotic factors than proximal cells (8). It is reported that the majority of apoptotic tubular cells are found in the distal and proximal tubules at 1 day after IR injury (25). Other studies showed no changes in Bax expression levels in the distal tubules, whereas the levels of Bcl-2, its heterodimeric partner, were increased (33).…”

Section: Discussionmentioning

confidence: 96%

Relaxin protects against renal ischemia-reperfusion injury

Yoshida

Kumagai

Kohsaka

et al. 2013

American Journal of Physiology-Renal Physiology

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Relaxin, a pregnancy hormone, has antiapoptotic and anti-inflammatory properties. The aim of this study was to determine the effects of relaxin on ischemia-reperfusion (IR)-induced acute kidney injury. Male rats underwent unilateral nephrectomy and contralateral renal IR (45 min of renal pedicle clamping). Rats were divided into three groups: 1) sham group, 2) IR group, and 3) IR-RLX group (rats treated with relaxin before ischemia). In this group, relaxin was infused at 500 ng/h via subcutaneous osmotic minipump for 24 h beginning 2 h before renal ischemia. At 24 h after reperfusion, renal function was assessed and kidneys were removed for analysis. There was no significant difference in blood pressure among the three groups. IR increased plasma levels of creatinine and urea nitrogen, and relaxin provided protection against the increases in these two parameters. Relaxin significantly decreased plasma TNF-α levels and renal TNF receptor 1 mRNA expression, compared with the IR group. Semiquantitative assessment of the histological lesions showed marked structural damage in IR rats compared with the IR-RLX rats. RLX significantly reduced apoptotic cell counts compared with the IR group. Overexpression of caspase-3 observed in the IR kidneys was reduced in the IR-RLX group. The results demonstrated that relaxin provided protection against IR-induced renal injury by reducing apoptosis and inflammation.

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“…This is the Wrst study showing that regular, moderate-intensity exercise could prevent the increase of apoptosis in the kidney. To date, apoptosis in renal tubular cells was well documented only in ischemic acute renal failure and in intoxications with some drugs, such as doxorubicin and cisplatin (Zhan et al 1999;Cao et al 2000;Oberbauer et al 2001;Hauser and Oberbauer 2002;Bhaskaran et al 2003). During ischemic renal injury, the occurrence of apoptosis was associated with reduced blood Xow, hypoxic conditions, and mild ATP depletion, followed by reperfusion (Padanilam 2003).…”

Section: Discussionmentioning

confidence: 97%

Effects of adaptive exercise on apoptosis in cells of rat renal tubuli

et al. 2006

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Regular exercise is known to improve physiological and functional capacity of many organs due to adaptive processes. We have previously shown that acute exercise in untrained rats results in apoptosis of renal tubular cells and that the apoptotic process seems to be associated with stimulation of angiotensin II, AT1 and AT2 receptors. In this study, we examined the influence of regular training on apoptosis and the role of angiotensin II receptors and antioxidant enzymes in mediating the adaptive response in renal tubular cells. We measured apoptosis, expression of AT1 and AT2 receptors, level of lipid peroxidation (TBARS) and activities of antioxidant enzymes, SOD, GPx and CAT in kidneys of sedentary rats that were exposed to acute exercise and rats that were trained for 8 weeks. In untrained animals, the acute exercise resulted in increased apoptosis and increased expression of AT1 and AT2 receptors in renal tubular cells, while in the rats exposed to the 8-week regular training, there were no changes in apoptosis nor AT1 and AT2 receptor expression as compared to the sedentary animals. The TBARS levels were significantly increased in acutely exercised rats, while in rats pre-exposed to the training they remained unchanged. The acute exercise, as well as regular training, did not change SOD, CAT or GPx activities. These findings suggested that the acute exercise-induced apoptosis in renal tubules could involve action of AT1 and AT2 receptors as well as oxidative stress, while the regular training was shown to prevent apoptosis in renal tubular cells via modulated expression of AT1 and AT2 receptors.

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Regulation of renal tubular cell apoptosis and proliferation after ischemic injury to a solitary kidney

Cited by 34 publications

References 25 publications

Involvement of Peripheral Benzodiazepine Receptor in the Oxidative Stress, Death-Signaling Pathways, and Renal Injury Induced by Ischemia-Reperfusion

Involvement of Peripheral Benzodiazepine Receptor in the Oxidative Stress, Death-Signaling Pathways, and Renal Injury Induced by Ischemia-Reperfusion

Relaxin protects against renal ischemia-reperfusion injury

Effects of adaptive exercise on apoptosis in cells of rat renal tubuli

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