The role of Bag2 in neurotoxicity induced by the anesthetic sevoflurane

Qi, Jinlian; Jia, Yingping; Wang, Wenhua; Lu, Haibing; Wang, Yuan; Li, Zhengchen

doi:10.1002/jcb.28029

Cited by 11 publications

(7 citation statements)

References 23 publications

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“…Numerous evidences have shown that BAG2 plays a substantial role in the pathogenesis of neurodegenerative diseases and neurotoxicity, such as Alzheimer's disease (14), Parkinson's disease (15), sevoflurane-induced neurotoxicity (16), etc. In recent years, the role of BAG2 in cancer has significantly attracted scholars' attention.…”

Section: Discussionmentioning

confidence: 99%

BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

et al. 2020

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Bcl2-associated athanogene (BAG)2 as a co-chaperone has been demonstrated to be involved in tumor growth and metastasis, but its biological function in gastric cancer remains unknown. Here, we reported that BAG2 was highly expressed in gastric cancer cell lines and tissues, indicating poor prognosis. High expression of BAG2 was significantly associated with T stage and differentiation level of gastric cancer (P < 0.001). Functional experiments revealed that BAG2 knockdown in gastric cancer cells inhibited the proliferation, invasion and migration of cells through AKT/mTOR and extracellular regulated kinase (ERK) pathways. Proteomic analysis identified that BAG2 may be involved in the regulation of mitogen-activated protein kinase (MAPK) pathway. In addition, immunoprecipitation showed that BAG2 could bind to ERK1/2. Luciferase reporter assay and Western blot verified that BAG2 was down-regulated by miR186. Taken together, our findings may reveal the basic function of BAG2 and uncover a potential therapeutic target for gastric cancer.

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Section: Discussionmentioning

confidence: 99%

BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

et al. 2020

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“…Preclinical study has shown that children exposed to sevoflurane demonstrated higher apoptosis status of neural stem cells [16]. Moreover, anesthetic sevoflurane could also induce neurotoxicity in neuronal cells with decreased cell viability and increased cell apoptosis [17]. The data from this study showed that exposure of the isolated neurons from neonatal rats to sevoflurane induced severely neurotoxicity with decreased cell viability and increased cell apoptosis.…”

Section: Discussionmentioning

confidence: 56%

“…Antioxidant defense was increased in children exposed to sevoflurane [16], and levels of reactive oxygen species were also accumulated in neonatal rats post sevoflurane exposure [4]. The reduction of reactive oxygen species was shown to be helpful for the amelioration of sevoflurane-induced neurotoxicity [17]. TRPM7 could release Zn 2+ through sensation of oxidative stress [18].…”

Section: Discussionmentioning

confidence: 99%

CD82 Aggravates Sevoﬂurane - Induced Neurotoxicity by Regulating TRPM7 in Developing Neurons

2020

Signa Vitae

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Background: Sevoflurane, a commonly used anesthetic in neonatal, could induce neurotoxicity in newborn animals. CD82 was found to be involved in age-related cognitive impairment. However, the role of CD82 in sevoflurane-induced neurotoxicity remains elusive. Methods: Hippocampal neurons were isolated from neonatal rats (postnatal day 1 or 2), and then exposed to 1.8 % sevoflurane for 6, 12, 24 or 48 hours. Neurons were pre-transfected with siRNA targeting CD82 (siCD82) or co-transfected with siTRPM7 (transient receptor potential melastatin 7) and pcDNA 3.1-CD82, and then exposed with sevoflurane (1.8%, 12 hours). Cell viability of the neurons was analyzed with MTT assay, and cell apoptosis was determined by flow cytometry. Protein expression was analyzed by western blot. Results: Sevoflurane exposure decreased cell viability of the developing hippocampal neurons in a time-dependent manner. Protein expressions of CD82 and TRPM7 were increased in neurons post sevoflurane exposure in a time-dependent manner. Pre-transfection of siCD82 attenuated sevoflurane-induced decrease in cell viability and increase in cell apoptosis in the neurons. Moreover, knockdown of CD82 reversed the promoting effects of sevoflurane on protein expression of cleaved TRPM7 and cleaved caspase-3. Over-expression of CD82 aggravated sevoflurane-induced decrease in cell viability and increase in cell apoptosis in neurons, while knockdown of TRPM7 counteracted with the effects of CD82 over-expression on sevoflurane-induced developing neurons. Conclusion: Sevoflurane exposure increased the expression of CD82 and TRPM7 in developing hippocampal neurons, decreased cell viability and promoted the cell apoptosis. Knockdown of CD82 partially ameliorated sevoflurane-induced neurotoxicity by down-regulation of cleaved TRPM7 in the developing neurons.

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“…As a commonly used anesthetic for general anesthesia, sevoflurane has been shown to be potentially neurotoxic to the developing brain (Qi et al, 2018; Yang et al, 2017). Ngb, an endogenous protein, has a neuroprotective effect on a variety of central nervous system diseases, such as stroke (Ren et al, 2015; Yu et al, 2018), ischemic and hypoxic brain injury (Wen et al, 2018) and neurodegenerative diseases (Liu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Neuroglobin protects offspring rats from neuronal damage induced by sevoflurane exposure to pregnant rats by inhibiting endogenous apoptosis

Zhang

Yang

Gao

et al. 2019

Intl J of Devlp Neuroscience

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As a general anesthesia drug, sevoflurane has been found to be potentially neurotoxic to the developing brain. Neuroglobin (Ngb) is a novel oxygen‐carrying globulin that has been demonstrated to have neuroprotective effects in a variety of central nervous system disorders. However, it is unclear whether Ngb has a protective effect on nerve damage caused by sevoflurane. Therefore, this study was designed to investigate the effect and related mechanisms of Ngb on neural injury induced by sevoflurane. Pregnant rats on gestational day 20 (G20) were exposed to 3.5% sevoflurane for two hours, which led to an increase of Ngb on the 0‐1st day after birth and decreased significantly on the 3rd day, while Cytochrome c increased from the 1 st day until the 7th day of offspring rats. Meanwhile, sevoflurane reduced Bcl‐2 and Hif‐1αand increased Bax and cleaved‐caspase 3 in the third day after birth. Hemin inhibits endogenous apoptosis by increasing Ngb and Hif‐1α. And increased Ngb improved the damage of long‐term learning and memory induced by sevoflurane and increased the number of neurons in the hippocampus. We concluded that Ngb can improve the neuronal injury induced by sevoflurane exposure by inhibiting apoptosis and increasing the number of neurons. And this protective effect of Ngb may be related to Hif‐1α signaling pathway. This finding may provide a novel therapeutic approach for sevoflurane ‐induced nerve damage.

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The role of Bag2 in neurotoxicity induced by the anesthetic sevoflurane

Cited by 11 publications

References 23 publications

BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

CD82 Aggravates Sevoﬂurane - Induced Neurotoxicity by Regulating TRPM7 in Developing Neurons

Neuroglobin protects offspring rats from neuronal damage induced by sevoflurane exposure to pregnant rats by inhibiting endogenous apoptosis

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