Prostaglandin E1 attenuates high glucose-induced apoptosis in proximal renal tubular cells by inhibiting the JNK/Bim pathway

Zhang, Yuhan; Zhang, Yaqin; Guo, Congcong; Wang, Li-Kang; Cui, Yujiao; Dong, Jianjun; Liao, Lin

doi:10.1038/s41401-019-0314-9

Cited by 26 publications

(16 citation statements)

References 46 publications

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“…Moreover, TUNEL analysis was used to further analyze the degree of cell damage in kidney tissues and the results indicated that apoptosis responses were observed signi cantly in PM 2.5 exposed rats. Previous studies suggested that apoptosis in renal tubular cells was considered as a causal factor in the development of kidney diseases/injury (Song et al, 2018;Zhang et al, 2019). Many in vivo and in vitro experiments have con rmed that PM 2.5 induced inappropriate apoptosis (too much) is one of the potential mechanisms of PM 2.5 health hazards (Liu et al, 2019;Wang et al, 2017b;Zhang et al, 2018a;Zhou et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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“…Lipofectamine 2000 was used to transfect miR-483-5p mimic or inhibitor when the cells grew to the logarithmic growth phase. After transfection for 6 hours, the cells were stimulated by replacing the medium containing high glucose (HG, 30 mM glucose) for 24 hours for subsequent experiments [22]. The normal glucose concentration of 5.5 mM glucose was used in the control group, and 5.5 mM glucose added 24.5 mM mannitol as the high osmotic (HO) pressure solution group.…”

Section: E L L Culture and Transfectionmentioning

confidence: 99%

miRNA-483–5p Targets HDCA4 to Regulate Renal Tubular Damage in Diabetic Nephropathy

et al. 2021

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This study was designed to evaluate the diagnostic value of miR-483–5p in diabetic nephropathy (DN), and its effect and mechanism on apoptosis and inflammation of human proximal renal tubular cells (HK2) induced by high glucose (HG). Thirty healthy controls, 30 types 2 diabetes mellitus (T2DM) patients, and 28 DN patients were enrolled. miR-483–5p mRNA levels in serum were analyzed by RT-qPCR assays. The receiver operating characteristic curve (ROC) was used to analyze the diagnostic value of miR-483–5p in DN. HK2 cells were induced by HG to establish an in vitro study model. CCK-8 and flow cytometry was used to detect cell viability, apoptosis, and reactive oxygen species (ROS) generation. Inflammation levels were measured by ELISA. Luciferase reporter assay was used to detect target genes of miR-483–5p. miR-483–5p was decreased in DN patients. The decreased level of miR-483–5p was positively correlated with estimated glomerular filtration rate (eGFR) and negatively correlated with proteinuria. miR-483–5p can significantly distinguish DN patients from healthy controls and T2DM and has a high diagnostic value. miR-483–5p decreased in HK2 cells induced by HG, and overexpression of miR-483–5p reversed HG-induced decreased cell activity, increased apoptosis, ROS production, and inflammation. Histone deacetylase 4 (HDCA4) was markedly increased in DN patients and HG-induced HK2 cells. miR-483–5p directly targeted HDCA4, and increasing miR-483–5p inhibited HDCA4 increased in HG-induced HK2. In conclusion, the results indicate that reduction of miR-483–5p has a high diagnostic value in DN, and overexpression of miR-483–5p has a certain protective effect on HK2 cells induced by HG by targeting HDCA4.

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“…Anisomycin was known to induce cell death and JNK activation was required for Anisomycin induced apoptosis ( Zhou et al, 2019 ; Zhang et al, 2020 ). We examined the p-JNK expression by western blot after the treatment of anisomycin in human breast cancer cell lines (MDA-MB-231, MDA-MB-436, BT549, Hs578T).…”

Section: Resultsmentioning

confidence: 99%

The Prognostic Significance of Anisomycin-Activated Phospho-c-Jun NH2-Terminal Kinase (p-JNK) in Predicting Breast Cancer Patients’ Survival Time

Chen

Kong

et al. 2021

Front. Cell Dev. Biol.

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This study aims to investigate the prognostic significance of p-JNK in breast cancer patients receiving neoadjuvant chemotherapy (NACT) and analyze the relationship between anisomycin, p-JNK. A total of 104 breast cancer patients had NACT were enrolled in this study. The western blot and immunohistochemistry assays were used to determine the protein expressions of p-JNK in human breast cancer cell lines and patients’ cancer tissues. The chi-square test and Fisher’s exact test were adopted to gauge the associations between breast cancer and clinicopathological variables by p-JNK expression, whereas the univariate and multivariate Cox proportional hazards regression models were used to analyze the prognostic value of p-JNK expression. The Kaplan-Meier plots and the log-rank test were adopted to determine patients’ disease-free survival (DFS) and overall survival (OS). Findings indicated that the p-JNK expression had prognostic significance in univariate and multivariate Cox regression survival analyses. Results of log-rank methods showed that: (1) the mean DFS and OS times in patients with high p-JNK expression were significantly longer than those in patients with low p-JNK expression (χ2 = 5.908, P = 0.015 and χ2 = 6.593, P = 0.010, respectively). p-JNK expression is a significant prognostic factor that can effectively predict the survival in breast cancer patients receiving NACT. Treatment with the JNK agonist anisomycin can induce apoptosis, lead to increased p-JNK expression and decreased p-STAT3 expression. Moreover, the p-JNK expression was inversely correlated with p-STAT3 expression.

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Prostaglandin E1 attenuates high glucose-induced apoptosis in proximal renal tubular cells by inhibiting the JNK/Bim pathway

Cited by 26 publications

References 46 publications

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

miRNA-483–5p Targets HDCA4 to Regulate Renal Tubular Damage in Diabetic Nephropathy

The Prognostic Significance of Anisomycin-Activated Phospho-c-Jun NH2-Terminal Kinase (p-JNK) in Predicting Breast Cancer Patients’ Survival Time

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