Role of Reactive Oxygen Species-Mediated Endoplasmic Reticulum Stress in Contrast-Induced Renal Tubular Cell Apoptosis

Yang, Yifei; Yang, Dingwei; Yang, Dingping; Jia, Ru; Ding, Guohua

doi:10.1159/000366063

Cited by 27 publications

(26 citation statements)

References 21 publications

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“…N-acetylcysteine also attenuated osmolar contrast-induced apoptosis of renal tubular cells by decreasing ROS levels and ER stress [31]. Similarly, flavonoids such as baicalin and quescetin reduced ER and oxidative stress, and they also ameliorated ischemia-reperfusion injury [32] or asymmetric dimethylarginine-induced apoptosis in glomerular endothelial cells [33].…”

Section: Antioxidative Chemicals and Proteins Relieve Endoplasmic Retmentioning

confidence: 93%

Endoplasmic reticulum stress in kidney function and disease

Taniguchi

Yoshida

2015

Current Opinion in Nephrology and Hypertension

112

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Section: Antioxidative Chemicals and Proteins Relieve Endoplasmic Retmentioning

confidence: 93%

Endoplasmic reticulum stress in kidney function and disease

Taniguchi

Yoshida

2015

Current Opinion in Nephrology and Hypertension

112

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“…There are concerns about its nephrotoxicity in administration (Golshahi et al, 2014). Contrast-induced nephropathy (CIN) is the third leading cause of hospitalacquired acute renal failure accounting for 10-12% of all causes of hospital-acquired renal failure (Yang et al, 2014). It causes a prolonged in-hospital stay and predicting a bad recovery (Hou et al, 1983;Briguori et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Contrast Media-Induced Renal Inflammation Is Mediated Through HMGB1 and Its Receptors in Human Tubular Cells

Guan

Chen

Zuo

et al. 2017

DNA and Cell Biology

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With the rapid development of imaging diagnosis and interventional therapy, contrast media (CM) are widely used in clinics. However, contrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure accounting for 10-12% of all causes of hospital-acquired renal failure. Recent study found that inflammation may participate in the pathogenesis of CIN, but the role of it remains unclear. HK-2 cells were treated with Iohexol, Urografin, and mannitol. Two types of CM increased the release of HMGB1 in cell supernatant accompanied by increased expression of TLR2 and CXCR4. Iohexol and Urografin also caused a significant increase in NF-κB followed by the release of IL-6 and MCP-1. To clarify the role of HMGB1, TLR2, and CXCR4, glycyrrhizin, anti-TLR2-IgG, and AMD3100 were used to inhibit HMGB1, TLR2, and CXCR4, respectively. Significant decrease in the expression of TLR2, CXCR4, nuclear NF-κB, and the release of IL-6 and MCP-1 were observed. These results indicate that TLR2 and CXCR4 signaling are involved in CM-induced HK-2 cell injury model in an HMGB1-dependent pathway, which may provide a new target for the prevention and the treatment of CIN.

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“…N-Acetyl-Lcysteine (NAC), a potent antioxidant, was used to alleviate ATO-induced ROS and the resulting oxidative DNA damage. Other reports and our previous studies demonstrated that 10 mM NAC is sufficient to reduce ROS level in various cell lines without affecting cell growth (Gu et al, 2015;Yang et al, 2014). Therefore, in this study, this NAC dosage was used and the results showed that it did not affect HepG2 cell growth (data not shown).…”

Section: Ros-mediated Dna Damage Was Responsible For the Ato-induced mentioning

confidence: 63%

The role of NF-κB in PARP-inhibitor-mediated sensitization and detoxification of arsenic trioxide in hepatocellular carcinoma cells

et al. 2015

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-The therapeutic efficacy of arsenic trioxide (ATO) for treatments of solid tumors is restricted by its drug resistance and chemotoxicity. In this study, we investigated ATO sensitization and detoxification effect of the Poly (ADP ribose) polymerase-1 (PARP-1) inhibitor 4-Amino-1,8-naphthalimide (4AN) in the hepatocellular carcinoma cell line HepG2. We firstly reported that ATO treatment induced the activation of Nuclear factor of κB (NF-κB) and its downstream anti-apoptosis and pro-inflammatory effectors in a PARP-1-dependent manner and thus conferred HepG2 cells with ATO resistance and toxicity. 4AN significantly suppressed the ATO-induced NF-κB activation, which promotes the apoptotic response and alleviates the inflammatory reaction induced by ATO, resulting in sensitization and detoxification against ATO. We also demonstrated that the ATO-induced activation of PARP-1 and NF-κB was closely associated with the oxidative DNA damage mediated by the generated reactive oxygen species (ROS). Furthermore, the attenuation of ATO-induced ROS and the resulting oxidative DNA damage by N-acetyl-L-cysteine (NAC), a potent antioxidant, significantly reduced the activation of PARP-1 and NF-κB in ATO-treated cells. Our study provides novel insights into the mechanism of the PARP-1-mediated NF-κB signaling pathway in ATO resistance and toxicity in anticancer treatments. This study also highlights the application potential of PARP-1 inhibitors in ATO-based anti-cancer treatments and in prevention of NF-κB-mediated therapeutic resistance and toxicity.

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Role of Reactive Oxygen Species-Mediated Endoplasmic Reticulum Stress in Contrast-Induced Renal Tubular Cell Apoptosis

Cited by 27 publications

References 21 publications

Endoplasmic reticulum stress in kidney function and disease

Endoplasmic reticulum stress in kidney function and disease

Contrast Media-Induced Renal Inflammation Is Mediated Through HMGB1 and Its Receptors in Human Tubular Cells

The role of NF-κB in PARP-inhibitor-mediated sensitization and detoxification of arsenic trioxide in hepatocellular carcinoma cells

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