Caffeic acid phenethyl ester against cadmium induced toxicity mediated by CircRNA modulates autophagy in HepG2 cells

Hao, Rili; Li, Feng; Song, Xubin; Tan, Xiao Di; Sun‐Waterhouse, Dongxiao

doi:10.1016/j.ecoenv.2020.110610

Cited by 24 publications

(12 citation statements)

References 32 publications

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“…Current research on circRNAs suggests that most circRNAs function as miRNA sponges and function by inhibiting the activity of target genes [ 30 ]. In recent years, an increasing number of studies have shown that circRNAs are involved in multiple cell biological processes, such as autophagy, cell proliferation, and apoptosis [ 31 , 32 ]. In our study, circGLI3 was involved in improving IPEC-J2 cell proliferation, regulation of intracellular antioxidant enzyme activity, and cellular ROS generation, indicating that circGLI3 may play a key role in protecting cells from oxidative damage during DQ-induced OS.…”

Section: Discussionmentioning

confidence: 99%

circGLI3 Inhibits Oxidative Stress by Regulating the miR-339-5p/VEGFA Axis in IPEC-J2 Cells

Wang

Zhang

et al. 2021

BioMed Research International

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As a new type of noncoding RNA, circular RNA (circRNA) is stable in cells and not easily degraded. This type of RNA can also competitively bind miRNAs to regulate the expression of their target genes. The role of circRNA in the mechanism of intestinal oxidative stress (OS) in weaned piglets is still unclear. In our research, diquat (DQ) was used to induce OS in small intestinal epithelial cells (IPEC-J2) to construct an OS cell model. Mechanistically, dual luciferase reporter assays, fluorescence in situ hybridization (FISH), and western blotting were performed to confirm that circGLI3 directly sponged miR-339-5p and regulated the expression of VEGFA. Overexpression of circGLI3 promoted IPEC-J2 cell proliferation, increased the proportion of S-phase cells ( P < 0.01 ), and reduced reactive oxygen species (ROS) generation when IPEC-J2 cells were subjected to OS. circGLI3 can increase the activity of glutathione peroxidase (GSH-Px) and the total antioxidant capacity (T-AOC) in IPEC-J2 cells and reduce the malondialdehyde (MDA) content and levels of inflammatory factors. Therefore, overexpression of circGLI3 reduced oxidative damage, whereas miR-339-5p mimic counteracted these effects. We identified a regulatory network composed of circGLI3, miR-339-5p, and VEGFA and verified that circGLI3 regulates VEGFA by directly binding miR-339-5p. The expression of VEGFA affects IPEC-J2 cell proliferation, cell cycle progression, and ROS content and changes the levels of antioxidant enzymes and inflammatory factors. This study reveals the molecular mechanism by which circGLI3 inhibits OS in the intestine of piglets and provides a theoretical basis for further research on the effect of OS on intestinal function.

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Section: Discussionmentioning

confidence: 99%

circGLI3 Inhibits Oxidative Stress by Regulating the miR-339-5p/VEGFA Axis in IPEC-J2 Cells

Wang

Zhang

et al. 2021

BioMed Research International

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“…Relative viability of PC12 cell was determined by the 3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide (MTT) assay to investigate the toxic effect of cadmium following previous method 27 . IC50 value is calculated using GraphPad Prism 7.0 (GraphPad Software, San Diego, CA, United States) by plotting concentration‐inhibition response curve.…”

Section: Methodsmentioning

confidence: 99%

“…Crystal violet staining was carried out following previous method 27 . The detailed experimental procedures are provided in the Supporting Information.…”

Section: Methodsmentioning

confidence: 99%

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Cadmium induces ferroptosis and apoptosis by modulating miR‐34a‐5p/Sirt1axis in PC12 cells

Hao

Song

et al. 2021

Environmental Toxicology

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Cadmium (Cd) is a potent neurotoxic metal present in the environment and food. In this study, CdCl2 (2 or 4 μM) induced cytotoxicity and neurotoxicity in PC12 cells, causing decreases in cell viability and NEP protein expression and increase in p‐tau protein expression. For the first time, CdCl2‐initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death‐related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl‐2 proteins. The molecular mechanisms leading to apoptosis and ferroptosis at least included the participation of the miR‐34a‐5p/Sirt1 axis, in which miR‐34a‐5p promoted CdCl2‐induced neurotoxicity through targeting Sirt1. Knocking out miR‐34a‐5p attenuated CdCl2‐induced damage of PC12 cells, cytotoxicity and neurotoxicity. This research provides the underlying molecular mechanisms of CdCl2‐induced damage and asserts the role of miRNAs as critical regulators.

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“…of the cells 32,33) . Ang II was known to increase the autophagy of GMCs 34,35) , and interestingly, in a recent work, calycosin has shown anti-autophagic effects in cerebral ischemic and reperfusion injury models 36) .…”

Section: Biological and Pharmaceutical Bulletin Advance Publicationmentioning

confidence: 99%

Calycosin may Alleviate Ang II-Induced Pro-proliferative Effects on Glomerular Mesangial Cells <i>via</i> Partially Inhibiting Autophagy and ERK Signaling Pathway

Ding

Luan

et al. 2020

Biological & Pharmaceutical Bulletin

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Over-expression of angiotensin II (Ang II) is an important reason for the development of chronic kidney disease. Calycosin is the active component of traditional Chinese medicine astragali radix. The present work aims to explore whether calycosin could affect the growth and apoptosis ability of the Ang II treated glomerular mesangial cells and the underlying mechanism. Human glomerular mesangial cells (GMCs) were cultured and treated by Ang II and 0, 0.1, 1 or 10 μM calycosin, and the viability and proliferation of the cells were determined by MTT and EdU staining; moreover, the apoptosis of the cells was examined by flow cytometry assay; furthermore, the expression levels of ERK, pERK , anti-apoptotic factor Bcl-2, as well as pro-apoptotic factor Bax have been examined by western blot methods; finally, the expression of autophagic markers in each group was examined by WB and immunocytochemistry methods. We found that Ang II increased viability and proliferation, meanwhile inhibited apoptosis of the GMCs; furthermore, 1 and 10 μM calycosin significantly inhibited the growth and promoted the apoptosis of the GMCs treated by Ang II; moreover, calycosin also inhibited ERK signaling in mesangial cells activated by Ang II treatment; Finally, calycosin could inhibit Ang II induced autophagy of GMCs in a dose-dependent manner. In conclusion, calycosin may alleviate Ang II-induced pro-proliferative and anti-apoptotic effects on glomerular mesangial cells at least partially via inhibiting autophagy and ERK signaling pathway, suggesting that calycosin may function as a potential alternative medication for the management of chronic kidney diseases.

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Caffeic acid phenethyl ester against cadmium induced toxicity mediated by CircRNA modulates autophagy in HepG2 cells

Cited by 24 publications

References 32 publications

circGLI3 Inhibits Oxidative Stress by Regulating the miR-339-5p/VEGFA Axis in IPEC-J2 Cells

circGLI3 Inhibits Oxidative Stress by Regulating the miR-339-5p/VEGFA Axis in IPEC-J2 Cells

Cadmium induces ferroptosis and apoptosis by modulating miR‐34a‐5p/Sirt1axis in PC12 cells

Calycosin may Alleviate Ang II-Induced Pro-proliferative Effects on Glomerular Mesangial Cells <i>via</i> Partially Inhibiting Autophagy and ERK Signaling Pathway

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