Cadmium-induced oxidative stress promotes apoptosis and necrosis through the regulation of the miR-216a-PI3K/AKT axis in common carp lymphocytes and antagonized by selenium

Zhang, Jiaqi; Zheng, Shufang; Wang, Shengchen; Liu, Qingqing; Xu, Shiwen

doi:10.1016/j.chemosphere.2020.127341

Cited by 94 publications

(34 citation statements)

References 50 publications

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“…20 human cells include the induction of oxidative stress, apoptosis, and invasion. 22,23 Oxidative stress was an important factor for heavy metal cytotoxicity in human cells. 12,22 As a crucial bio-signaling molecule, ROS tumor necrosis factor-α (TNF-α), and activated nuclear factor-κB (NF-κB) inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

“…22,23 Oxidative stress was an important factor for heavy metal cytotoxicity in human cells. 12,22 As a crucial bio-signaling molecule, ROS tumor necrosis factor-α (TNF-α), and activated nuclear factor-κB (NF-κB) inflammatory responses. 28 Increasing evidence indicate that the toll-like receptors (TLRs) and SMAD family proteins play an important role in the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

“…These results proved that Cd cytotoxicity in HTR‐8/SVneo cells was caused by reducing cell viability and adhesion capacity, inhibiting the proliferation, and injuring the nucleus and organelles. It has been certified that the mechanisms of Cd toxicity in human cells include the induction of oxidative stress, apoptosis, and invasion 22,23 …”

Section: Discussionmentioning

confidence: 99%

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Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR‐8/SVneo cells

Liao

Zheng

et al. 2021

Environmental Toxicology

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The accumulation of cadmium (Cd) in the human body through food chain can lead to adverse pregnancy outcomes. In this study, Cd cytotoxicity and its mechanisms in HTR-8/SVneo cells were investigated. Cd disrupted the cellular submicrostructure and inhibited the cell viability in a time-and dose-dependent manner. The levels of reactive oxygen species, malondialdehyde content, and the activities of glutathione peroxidase (GSH-Px) and total superoxode dismutase (T-SOD) were concentrationdependently increased by Cd. In addition, Cd dose-dependently inducedcell apoptosis and decreased cell migration and invasion capacities. Finally, Cd significantly upregulated all the genes related to oxidative stress (SOD1, ROS1, and HSPA6), inflammatory response, cell cycle, apoptosis, and migration and invasion. This study will provide insights into the prevention and treatment of pregnancy-related diseases caused by Cd intoxication.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR‐8/SVneo cells

Liao

Zheng

et al. 2021

Environmental Toxicology

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“…The AO penetrates the intact cell membrane and inserts nuclear DNA into the cell, causing emission of a bright green fluorescence. The EB can only penetrate cells with damaged membranes, embed nuclear DNA in agar, and emit orange fluorescence (18)(19)(20). Among them, normal cells appeared green.…”

Section: Apoptosis Of Fibroblasts After E2 Stimulationmentioning

confidence: 99%

Therapeutic Effects of 17β-Estradiol on Pelvic Organ Prolapse by Inhibiting Mfn2 Expression: An In Vitro Study

Wang

Xiao

et al. 2020

Front. Endocrinol.

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ObjectiveTo assess the effects of 17β-estradiol (E2) on proliferation, apoptosis, and protein expressions of fibroblasts at different concentrations and time intervals to reveal the mechanism of E2 in the treatment of pelvic organ prolapse (POP).Study DesignThe uterosacral ligament fibroblasts were collected from seven POP patients for primary culture of fibroblasts. The culture media containing 0, 10-6, 10-7, 10-8, and 10-9 mol/L E2 were used for 24, 48, 72, and 96 h.Main Outcome MeasuresThe cells were collected for cell counting kit-8 (CCK-8), apoptosis, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blotting assays.ResultsCompared with the control group, in the values of fibroblasts cultured in 10-8 mol/L E2 for 72 h, the proliferation, mRNA and protein expression of Mitofusin-2 (Mfn2) separately increased (P < 0.05), decreased (P<0.001) and decreased (P<0.001). However, the expression level of procollagen 1A1/1A2/3A1 and cyclinD1 markedly increased (P<0.001, all), which was consistent with the results of protein level. What’s more, the expression of estrogen receptor α(ERα), estrogen receptor β(ERβ) and G protein-coupled receptor 30(GPR30) were significantly increased in 10-8 mol/L E2 group.ConclusionsE2 can inhibit the progress of POP by inhibiting the expression level of Mfn2, as well as promoting expression of procollagens and proliferation of fibroblasts. This effect is time- and concentration-dependent. Only when the estrogen concentration reaches 10-8 mol/L, the therapeutic effect is the greatest after 72 h.

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“…It has been found that Bcl-2 has anti apoptotic effects and Bax has pro-apoptotic effects (Adams and Cory, 1998). Numerous researches have shown that AKT protein is a major regulator involved in the transcriptional regulation of Bcl-2 (Ghosh et al, 2013;Chen et al, 2020;Zhang et al, 2020). AKT activation increases the expression of the Bcl-2 through phosphorylation of cyclic AMP response binding protein (Pugazhenthi et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Grape Seed Proanthocyanidin Extract Ameliorates Cardiac Remodelling After Myocardial Infarction Through PI3K/AKT Pathway in Mice

et al. 2020

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Myocardial infarction is one of the most serious fatal diseases in the world, which is due to acute occlusion of coronary arteries. Grape seed proanthocyanidin extract (GSPE) is an active compound extracted from grape seeds that has anti-oxidative, anti-inflammatory and anti-tumor pharmacological effects. Natural products are cheap, easy to obtain, widely used and effective. It has been used to treat numerous diseases, such as cancer, brain injury and diabetes complications. However, there are limited studies on its role and associated mechanisms in myocardial infarction in mice. This study showed that GSPE treatment in mice significantly reduced cardiac dysfunction and improved the pathological changes due to MI injury. In vitro, GSPE inhibited the apoptosis of H9C2 cells after hypoxia culture, resulting in the expression of Bax decreased and the expression of Bcl-2 increased. The high expression of p-PI3K and p-AKT was detected in MI model in vivo and in vitro. The use of the specific PI3K/AKT pathway inhibitor LY294002 regressed the cardio-protection of GSPE. Our results showed that GSPE could improve the cardiac dysfunction and remodeling induced by MI and inhibit cardiomyocytes apoptosis in hypoxic conditions through the PI3K/AKT signaling pathway.

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Cadmium-induced oxidative stress promotes apoptosis and necrosis through the regulation of the miR-216a-PI3K/AKT axis in common carp lymphocytes and antagonized by selenium

Cited by 94 publications

References 50 publications

Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR‐8/SVneo cells

Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR‐8/SVneo cells

Therapeutic Effects of 17β-Estradiol on Pelvic Organ Prolapse by Inhibiting Mfn2 Expression: An In Vitro Study

Grape Seed Proanthocyanidin Extract Ameliorates Cardiac Remodelling After Myocardial Infarction Through PI3K/AKT Pathway in Mice

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