Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death

Jiang, Yu; Sheng, Chang; Luo, Kun; Ding, Jian; Nan, Qi Yan; Piao, Shang Guo; Xuan, Mei Ying; Zheng, Hongliang; Jin, Ji Zhe; Lee, Jung Pyo; Chung, Byung Ha; Choi, Bum Soon; Yang, Chul Woo; Li, Can

doi:10.3904/kjim.2021.326

Cited by 5 publications

(3 citation statements)

References 38 publications

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“…This finding suggests that CTLA4-Ig has a direct effect on protecting TAC-induced renal injury. Our study showed that TAC causes prominent renal damage, which is in accordance with previous studies [20][21][22]. CTLA4-Ig, however, protected against renal injury and oxidative stress from TAC stimulation, indicating that CTLA4-Ig can protect the kidneys from TAC-induced damage in vivo.…”

Section: Discussionsupporting

confidence: 92%

CTLA4-Ig protects tacrolimus-induced oxidative stress via inhibiting the AKT/FOXO3 signaling pathway in rats

Jin¹,

Shen²,

Xu³

et al. 2023

Korean J Intern Med

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Background/Aims: Although the conversion from tacrolimus (TAC) to cytotoxic T-lymphocyte-associated antigen 4-immunoglobulin (CTLA4-Ig) is effective in reducing TAC-induced nephrotoxicity, it remains unclear whether CTLA4-Ig has a direct effect on TAC-induced renal injury. In this study, we evaluated the effects of CTLA4-Ig on TAC-induced renal injury in terms of oxidative stress.Methods: In vitro study was performed to assess the effect of CTLA4-Ig on TAC-induced cell death, reactive oxygen species (ROS), apoptosis, and the protein kinase B (AKT)/forkhead transcription factor (FOXO) 3 pathway in human kidney 2 cells. In the in vivo study, the effect of CTLA4-Ig on TAC-induced renal injury was evaluated using renal function, histopathology, markers of oxidative stress (8-hydroxy-2’-deoxyguanosine) and metabolites (4-hydroxy-2-hexenal, catalase, glutathione S-transferase, and glutathione reductase), and activation of the AKT/FOXO3 pathway with insulin-like growth factor 1 (IGF-1).Results: CTLA4-Ig significantly decreased cell death, ROS, and apoptosis caused by TAC. TAC treatment increased apoptotic cell death and apoptosis-related proteins (increased Bcl-2-associated X protein and caspase-3 and decreased Bcl-2), but it was reversed by CTLA4-Ig treatment. The activation of p-AKT and p-FOXO3 by TAC decreased with CTLA4-Ig treatment. TAC-induced renal dysfunction and oxidative marker levels were significantly improved by CTLA4-Ig in vivo. Concomitant IGF-1 treatment abolished the effects of CTLA4-Ig.Conclusions: CTLA4-Ig has a direct protective effect on TAC-induced renal injury via the inhibition of AKT/FOXO3 pathway.

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Section: Discussionsupporting

confidence: 92%

CTLA4-Ig protects tacrolimus-induced oxidative stress via inhibiting the AKT/FOXO3 signaling pathway in rats

Jin¹,

Shen²,

Xu³

et al. 2023

Korean J Intern Med

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“…Interestingly, Zhong et al showed that inhibition of ER stress with 4-phenylbutyric acid (4-PBA) mitigates kidney damage and mitochondrial apoptosis due to nephrotoxicity of 3-monochloropropane diol (3-MCPD) [82]. Another study showed that nicotine (NIC), a toxic component of smoke, can accelerate the progression of pre-existing kidney damage by disrupting mitochondrial structural integrity, triggering ER stress, and altering the expression of mitochondrial and ER stress genes [83]. Overall, these findings suggest that the crosstalk between ER and mitochondria has important implications in kidney disorders and that the regulation of both may be a potential therapeutic strategy for kidney protection.…”

Section: Er Crosstalk With Other Organelles In Kidney Diseases Er Cro...mentioning

confidence: 99%

Research progress on endoplasmic reticulum homeostasis in kidney diseases

Huang

Chen

et al. 2023

Cell Death Dis

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The endoplasmic reticulum (ER) plays important roles in biosynthetic and metabolic processes, including protein and lipid synthesis, Ca2+ homeostasis regulation, and subcellular organelle crosstalk. Dysregulation of ER homeostasis can cause toxic protein accumulation, lipid accumulation, and Ca2+ homeostasis disturbance, leading to cell injury and even death. Accumulating evidence indicates that the dysregulation of ER homeostasis promotes the onset and progression of kidney diseases. However, maintaining ER homeostasis through unfolded protein response, ER-associated protein degradation, autophagy or ER-phagy, and crosstalk with other organelles may be potential therapeutic strategies for kidney disorders. In this review, we summarize the recent research progress on the relationship and molecular mechanisms of ER dysfunction in kidney pathologies. In addition, the endogenous protective strategies for ER homeostasis and their potential application for kidney diseases have been discussed.

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“…Nicotine can increase malignancy through EMT in lung cancer ( Dasgupta et al, 2009 ; Pillai et al, 2015 ; Zhang et al, 2016 ; Du et al, 2018 ). Nicotine can directly induce ER stress response ( Pelissier-Rota et al, 2015 ; Barra et al, 2017 ; Gonzales et al, 2021 ; Jiang et al, 2021 ). In our previous study, we confirmed that nicotine concentration and time dependently increased the expression of ER stress associated apoptosis marker in human bronchial epithelial cells ( Lin et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Bronchial Epithelial Cell Epithelial Mesenchymal Transition Through Regulating Endoplasm Reticulum Stress

Lin

Liao

Zhang

et al. 2022

Front. Mol. Biosci.

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Epithelial mesenchymal transition (EMT) is a contributing factor in remodeling events of chronic obstructive pulmonary disease (COPD). Hydrogen sulfide (H2S) has been implicated in the pathogenesis of COPD, but the effect of H2S in regulating EMT and the underlying mechanisms is not clear. In this study, we assessed endoplasmic reticulum (ER) stress markers, EMT markers and associated signal molecules in rat lungs, bronchial epithelial cells, and human peripheral lung tissues to investigate the effect of H2S in regulating EMT and the underlying mechanisms. We found that EMT and ER stress occurred in lung epithelial cells, especially in the bronchial epithelial cells of smokers and COPD patients. In cigarette smoke (CS)-exposed rats, intraperitoneal injection of NaHS significantly alleviated CS-induced lung tissue damage, small airway fibrosis, ER stress, and EMT, while intraperitoneal injection of propargylglycine (cystathionine-gamma-lyase inhibitor) aggravated these effects induced by CS. In the nicotine-exposed 16HBE cells, an appropriate concentration of H2S donor not only inhibited nicotine-induced ER stress, but also inhibited nicotine-induced enhancement of cell migration ability and EMT. ER stress nonspecific inhibitors taurine and 4-phenyl butyric acid also inhibited nicotine-induced enhancement of cell migration ability and EMT. Both H2S and inositol-requiring enzyme 1 (IRE1) activation inhibitor 4μ8C inhibited nicotine-induced activation of IRE1, Smad2/3 and EMT. These results suggest that H2S inhibits CS- or nicotine-induced ER stress and EMT in bronchial epithelial cells and alleviates CS-induced lung tissue damage and small airway fibrosis. The IRE1 signal pathway and Smad2/3 may be responsible for the inhibitory effect of H2S.

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Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death

Cited by 5 publications

References 38 publications

CTLA4-Ig protects tacrolimus-induced oxidative stress via inhibiting the AKT/FOXO3 signaling pathway in rats

CTLA4-Ig protects tacrolimus-induced oxidative stress via inhibiting the AKT/FOXO3 signaling pathway in rats

Research progress on endoplasmic reticulum homeostasis in kidney diseases

Hydrogen Sulfide Inhibits Bronchial Epithelial Cell Epithelial Mesenchymal Transition Through Regulating Endoplasm Reticulum Stress

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