Pink1/Parkin-mediated mitophagy play a protective role in cisplatin induced renal tubular epithelial cells injury

Zhao, Chuanyan; Chen, Zhuyun; Xu, Xueqiang; An, Xiaofei; Duan, Suyan; Huang, Zhimin; Zhang, Chengning; Wu, Lin; Zhang, Bo; Zhang, Aihua; Xing, Changying; Yuan, Yanggang

doi:10.1016/j.yexcr.2016.12.015

Cited by 81 publications

(59 citation statements)

References 27 publications

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“…Mitophagy plays an important role in the clearance of damaged mitochondria (Linkermann et al, 2014). The reduction of mitophagy significantly exacerbated cell apoptosis and tissue damage of AKI (Zhao et al, 2017;Tang et al, 2018;Yang et al, 2018). In the present study, activation of mitophagy was found in HK-2 cells after I/R treatment.…”

Section: Discussionsupporting

confidence: 55%

“…Many studies have reported that PINK1/Parkin signaling controls the selective degradation of dysfunctional mitochondria by mitophagy in acute kidney disease (Zhao et al, 2017;Tang et al, 2018;Lin et al, 2019). In healthy mitochondria, PINK1 is constitutively inserted into the mitochondria inner membrane and rapidly degraded by proteolysis to keep a low level of expression.…”

Section: Discussionmentioning

confidence: 99%

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Augmenter of Liver Regeneration Protects Renal Tubular Epithelial Cells From Ischemia-Reperfusion Injury by Promoting PINK1/Parkin-Mediated Mitophagy

et al. 2020

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Ischemia-reperfusion (I/R) is the most common cause of acute kidney injury (AKI) and can induce apoptosis in renal epithelial tubule cells. Mitochondrial dysfunction is one of the main reasons for I/R-induced apoptosis. Accumulating evidence suggests that PINK1/Parkin-mediated mitophagy possibly plays a renoprotective role in kidney disease by removing impaired mitochondria and preserving a healthy population of mitochondria. Our previous study showed that augmenter of liver regeneration (ALR) alleviates tubular epithelial cells apoptosis in rats with AKI, although the specific mechanism remains unclear. In this study, we investigated the role of ALR in I/Rinduced mitochondrial pathway of apoptosis. We knocked down ALR with short hairpin RNA lentiviral and established an I/R model in human kidney proximal tubular (HK-2) cells in vitro. We observed that the knockdown of ALR aggravated mitochondrial dysfunction and increased the mitochondrial reactive oxygen species (ROS) levels, leading to an increase in cell apoptosis via inhibition of mitophagy. We also found that the PINK1/Parkin pathway was activated by I/R via confocal microscopy and Western blot. Furthermore, the knockdown of ALR suppressed the activation of PINK1 and Parkin. These findings collectively indicate that ALR may protect HK-2 cells from I/R injury by promoting mitophagy, and the mechanism by which ALR regulates mitophagy seems to be related to PINK1 and Parkin. Consequently, ALR may be used as a potential therapeutic agent for AKI in the future.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Augmenter of Liver Regeneration Protects Renal Tubular Epithelial Cells From Ischemia-Reperfusion Injury by Promoting PINK1/Parkin-Mediated Mitophagy

et al. 2020

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“…Yuan's group reported that PINK1/Parkin‐mediated mitophagy was induced due to cisplatin exposure. In cultured human renal proximal tubular cells, they knocked down PINK1/Parkin and found mitochondrial function was bothered; mitophagy was inhibited, thus resulting in increased cell injury (Zhao et al, ). Our results were consistent with these findings in other inflammation diseases.…”

Section: Discussionmentioning

confidence: 99%

Activation of mitophagy in inflamed odontoblasts

Yang

Duan

et al. 2019

Oral Diseases

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Objectives Mitophagy is an important mitochondrial quality control mechanism. In this study, we investigated the mitochondrial damage and mitophagy occurred in inflammatory human dental pulp and lipopolysaccharide‐stimulated preodontoblasts. Materials and Methods In dental pulp tissues and lipopolysaccharide‐stimulated preodontoblasts, immunofluorescences and Western blot were performed to detect the expression of mitochondrial and mitophagy‐related proteins, and autophagy markers were also examined. Reactive oxygen species generated by mitochondria were examined by MitoSOX. Transmission electron microscope (TEM) was used to examine the morphology of mitochondria in lipopolysaccharide‐stimulated preodontoblasts. Results The active fission activity of mitochondria and mitophagy in inflammatory dental pulp was observed. In lipopolysaccharide‐treated preodontoblasts, mitophagy‐related proteins were also upregulated. Moreover, increased reactive oxygen species in the inflamed preodontoblasts were observed. Additionally, single‐membrane autolysosomes containing partially degraded mitochondria with swollen inner membranes in lipopolysaccharide‐treated preodontoblasts were observed by TEM. Conclusions These results indicate that mitochondria were damaged and mitophagy might be activated to degrade impaired mitochondria in inflamed odontoblasts.

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“…Although initially identified in familial Parkinson’s disease [40], recent studies showed that autophagy in kidney was of great significance for the homeostasis of renal tubular [41, 42]. Autophagy and mitophagy have been well studied in renal ischemia-reperfusion, sepsis and cisplatin induced acute kidney injury [15, 43-45]. However, there are few researches on the effect and possible disparities of LOCM and IOCM on mitophagy and its role in renal injury induced by iodinated contrast media.…”

Section: Discussionmentioning

confidence: 99%

“…Mitochondrial dysfunction had been implicated in a series of diseases [15, 16]. A previous study has proved that mitophagy plays a protective role in cisplatin induced renal tubular epithelial cells injury [15].…”

Section: Introductionmentioning

confidence: 99%

Mitophagy Plays a Protective Role in Iodinated Contrast-Induced Acute Renal Tubular Epithelial Cells Injury

Lei

Zhao

Tang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Contrast induced-acute kidney injury (CI-AKI) is one of the most common causes of acute kidney injury (AKI) in hospitalized patients. Mitophagy, the selective elimination of mitochondria via autophagy, is an important mechanism of mitochondrial quality control in physiological and pathological conditions. In this study, we aimed to determine effects of iohexol and iodixanol on mitochondrial reactive oxygen species (ROS), mitophagy and the potential role of mitophagy in CI-AKI cell models. Methods: Cell viability was measured by cell counting kit-8. Cell apoptosis, mitochondrial ROS and mitochondrial membrane potential were detected by western blot, MitoSOX fluorescence and TMRE staining respectively. Mitophagy was detected by the colocalization of LC3-FITC with MitoTracker Red, western blot and electronic microscope. Results: The results showed that mitophagy was induced in human renal tubular cells (HK-2 cells) under different concentrations of iodinated contrast media. Mitochondrial ROS displayed increased expression after the treatment. Rapamycin (Rap) enhanced mitophagy and alleviated contrast media induced HK-2 cells injury. In contrast, autophagy inhibitor 3-methyladenine (3-MA) down-regulated mitophagy and aggravated cells injury. Conclusions: Together, our finding indicates that iohexol and iodixanol contribute to the generation of mitochondrial ROS and mitophagy. The enhancement of mitophagy can effectively protect the kidney from iodinated contrast (iohexol)-induced renal tubular epithelial cells injury.

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Pink1/Parkin-mediated mitophagy play a protective role in cisplatin induced renal tubular epithelial cells injury

Cited by 81 publications

References 27 publications

Augmenter of Liver Regeneration Protects Renal Tubular Epithelial Cells From Ischemia-Reperfusion Injury by Promoting PINK1/Parkin-Mediated Mitophagy

Augmenter of Liver Regeneration Protects Renal Tubular Epithelial Cells From Ischemia-Reperfusion Injury by Promoting PINK1/Parkin-Mediated Mitophagy

Activation of mitophagy in inflamed odontoblasts

Mitophagy Plays a Protective Role in Iodinated Contrast-Induced Acute Renal Tubular Epithelial Cells Injury

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