Ischemia-reperfusion injury: Biochemical alterations in peroxisomes of rat kidney

Gulati, Shilpa; Singh, Avtar; Irazú, Carlos E.; Orak, John K.; Rajagopalan, P. R.; Fitts, Charles T.; Singh, Inderjit

doi:10.1016/0003-9861(92)90492-f

Cited by 62 publications

(30 citation statements)

References 33 publications

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“…Previous studies documented that peroxisome number and/or function were damaged in the kidneys of mice undergoing I/R injury (13). In the present study, however, we failed to demonstrate a beneficial effect of Sirt1 on the development of AKI when induced by I/R injury (Fig.…”

Section: Discussioncontrasting

confidence: 67%

“…Furthermore, Sirt1 has been reported to preserve mitochondria function by inducing PGC-1␣, which increases mitochondrial number (10). Because both peroxisome and mitochondrial functions are compromised by pathophysiological conditions, including cisplatin-induced (11,12) and ischemic/reperfusion (I/R)-induced acute kidney injury (AKI) (13,14), it is anticipated that Sirt1 is capable of alleviating renal injury by modulating peroxisome and mitochondrial function.…”

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confidence: 99%

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Kidney-specific Overexpression of Sirt1 Protects against Acute Kidney Injury by Retaining Peroxisome Function

Hara

Wakino

Yoshioka

et al. 2010

Journal of Biological Chemistry

209

174

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Sirt1, a NAD-dependent protein deacetylase, is reported to regulate intracellular metabolism and attenuate reactive oxidative species (ROS)-induced apoptosis leading to longevity and acute stress resistance. We created transgenic (TG) mice with kidney-specific overexpression of Sirt1 using the promoter sodium-phosphate cotransporter IIa (Npt2) driven specifically in proximal tubules and investigated the kidney-specific role of Sirt1 in the protection against acute kidney injury (AKI). We also elucidated the role of number or function of peroxisome and mitochondria in mediating the mechanisms for renal protective effects of Sirt1 in AKI. Cisplatin-induced AKI decreased the number and function of peroxisomes as well as mitochondria and led to increased local levels of ROS production and renal tubular apoptotic cells. TG mice treated with cisplatin mitigated AKI, local ROS, and renal tubular apoptotic tubular cells. Consistent with these results, TG mice treated with cisplatin also exhibited recovery of peroxisome number and function, as well as rescued mitochondrial function; however, mitochondrial number was not recovered. Immunoelectron microscopic findings consistently demonstrated that the decrease in peroxisome number by cisplatin in wild type mice was restored in transgenic mice. In HK-2 cells, a cultured proximal tubule cell line, overexpression of Sirt1 rescued the cisplatin-induced cell apoptosis through the restoration of peroxisome number, although the mitochondria number was not restored. These results indicate that Sirt1 overexpression in proximal tubules rescues cisplatin-induced AKI by maintaining peroxisomes number and function, concomitant up-regulation of catalase, and elimination of renal ROS levels. Renal Sirt1 can be a potential therapeutic target for the treatment of AKI.

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Section: Discussioncontrasting

confidence: 67%

mentioning

confidence: 99%

Kidney-specific Overexpression of Sirt1 Protects against Acute Kidney Injury by Retaining Peroxisome Function

Hara

Wakino

Yoshioka

et al. 2010

Journal of Biological Chemistry

209

174

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“…53 Furthermore, peroxisomes are induced by conditions such as hypolipidemic drugs treatment, 50 cold shock, 54 and ischemia and reperfusion. 55 Under these conditions, an additional catalase peak is present in the lighter part of the gradient. Therefore, lighter peroxisomes may represent peroxisomes in the process of maturation, 50,53 or peroxisomal particles generated due to fragmentation of peroxisomal reticulum.…”

Section: Discussionmentioning

confidence: 98%

Endotoxin induces structure-function alterations of rat liver peroxisomes: Kupffer cells released factors as possible modulators

et al. 2000

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We report that endotoxin treatment results in decreased amounts of peroxisomes as well as changes in structure and function of peroxisomal membranes. Peroxisomes isolated from the liver of control and treated animals showed a marked decrease in total protein, but no significant alteration in the sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) protein profile. However, the Western blot study of the peroxisomal ␤-oxidation enzymes and catalase showed an increase in those enzymes in the peroxisomal peak of normal density in endotoxin-treated rats.

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“…Gulati et al showed for the first time that renal ischemia-reperfusion is accompanied by functional and structural damage of peroxisomes (33). Almost 90% of cellular catalase activity is localized to peroxisomes.…”

Section: Ischemic Akimentioning

confidence: 99%

Peroxisomes and Kidney Injury

Vasko

2016

Antioxidants & Redox Signaling

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Significance: Peroxisomes are organelles present in most eukaryotic cells. The organs with the highest density of peroxisomes are the liver and kidneys. Peroxisomes possess more than fifty enzymes and fulfill a multitude of biological tasks. They actively participate in apoptosis, innate immunity, and inflammation. In recent years, a considerable amount of evidence has been collected to support the involvement of peroxisomes in the pathogenesis of kidney injury. Recent Advances: The nature of the two most important peroxisomal tasks, betaoxidation of fatty acids and hydrogen peroxide turnover, functionally relates peroxisomes to mitochondria. Further support for their communication and cooperation is furnished by the evidence that both organelles share the components of their division machinery. Until recently, the majority of studies on the molecular mechanisms of kidney injury focused primarily on mitochondria and neglected peroxisomes. Critical Issues: The aim of this concise review is to introduce the reader to the field of peroxisome biology and to provide an overview of the evidence about the contribution of peroxisomes to the development and progression of kidney injury. The topics of renal ischemia-reperfusion injury, endotoxin-induced kidney injury, diabetic nephropathy, and tubulointerstitial fibrosis, as well as the potential therapeutic implications of peroxisome activation, are addressed in this review. Future Directions: Despite recent progress, further studies are needed to elucidate the molecular mechanisms induced by dysfunctional peroxisomes and the role of the dysregulated mitochondria-peroxisome axis in the pathogenesis of renal injury. Antioxid. Redox Signal. 25, 217-231.

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Ischemia-reperfusion injury: Biochemical alterations in peroxisomes of rat kidney

Cited by 62 publications

References 33 publications

Kidney-specific Overexpression of Sirt1 Protects against Acute Kidney Injury by Retaining Peroxisome Function

Kidney-specific Overexpression of Sirt1 Protects against Acute Kidney Injury by Retaining Peroxisome Function

Endotoxin induces structure-function alterations of rat liver peroxisomes: Kupffer cells released factors as possible modulators

Peroxisomes and Kidney Injury

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