Downregulation of survivin regulates adult hippocampal neurogenesis and apoptosis, and inhibits spatial learning and memory following traumatic brain injury

Zhang, Z; Wang, H; Jin, Zhangning; Cai, Xinwang; Gao, Nannan; Cui, Xiaoteng; Liu, P; Zhang, J; Shen, Yang; Yang, Xinyu

doi:10.1016/j.neuroscience.2015.05.025

Cited by 17 publications

(12 citation statements)

References 42 publications

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“…Survivin is an important member of the inhibitor of apoptosis protein family that regulates apoptosis and cell division ( 46 ). Previous research has demonstrated that the expression of survivin in embryonic development promotes tissue stability and differentiation ( 47 , 48 ).…”

Section: Discussionmentioning

confidence: 99%

Lycium�barbarum polysaccharides protect human trophoblast HTR8/SVneo cells from hydrogen peroxide‑induced oxidative stress and apoptosis

Ding

Yang

et al. 2018

Mol Med Report

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Pregnancy complications are associated with abnormal cytotrophoblast differentiation and invasion. Hydrogen peroxide (H2O2) is an important mediator of oxidative ischemia/reperfusion stress in the placenta. Lycium barbarum polysaccharides (LBP) have been demonstrated to counteract oxidative free radicals. The effects of LBP in trophoblast HTR8/SVneo cells injured with H2O2 were examined. A cell counting kit-8 assay was performed to detect the effect of LBP at different concentrations on the proliferative ability of H2O2 injured trophoblast cells. Flow cytometry was used to determine the levels of reactive oxygen species (ROS), mitochondria membrane potential (MMP) disruption and apoptosis. Superoxide dismutase (SOD) activity and lactate dehydrogenase (LDH) leakage into the supernatant was detected by ultraviolet spectrophotometry. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were performed to detect the expression of apoptosis-associated factors, including survivin, hypoxia inducible factor 1-α (HIF1-α), Bcl-2 apoptosis regulator (Bcl-2), Bcl-2 associated X apoptosis regulator (Bax). The results revealed that LBP protected the proliferative ability of trophoblast cells injured with H2O2 in a dose-dependent manner. LBP inhibited the oxidative stress induced by H2O2, by reducing ROS and LDH levels and increasing SOD activity. Additionally, LBP decreased MMP disruption and cell apoptosis induced by H2O2, by increasing the mRNA and protein expression of survivin, HIF1-α and Bcl-2 and decreasing Bax expression. Therefore, it was concluded that LBP protected human trophoblast cells from H2O2-induced oxidative stress and cell apoptosis via regulation of apoptosis-associated factor expression. It will provide a novel strategy for the treatment of pregnancy complications.

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Section: Discussionmentioning

confidence: 99%

Lycium�barbarum polysaccharides protect human trophoblast HTR8/SVneo cells from hydrogen peroxide‑induced oxidative stress and apoptosis

Ding

Yang

et al. 2018

Mol Med Report

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“…Concomitantly, propofol also induced YAP nuclear translocation ( Figure 4(b) ). Activated YAP stimulates the transcription of genes that promote cellular survival, such as survivin and Bcl2 [ 12 , 27 , 28 ]. We further tested the roles of propofol in expression of survivin and Bcl2.…”

Section: Resultsmentioning

confidence: 99%

Propofol Protects Hippocampal Neurons from Hypoxia‐Reoxygenation Injury by Decreasing Calcineurin‐Induced Calcium Overload and Activating YAP Signaling

Liang

et al. 2018

Oxidative Medicine and Cellular Longevity

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Objectives Propofol is a popular anesthetic drug that is neuroprotective. However, the mechanisms of propofol for hippocampal neuroprotection remain elusive. This study is aimed at investigating the neuroprotective effect and mechanism of propofol in hippocampal neurons exposed to ischemia-reperfusion (I/R) injury. Methods Hypoxia-reoxygenated (H/R) HT-22 cells were used to mimic I/R injury of the hippocampus in vitro. An MTT assay was used to determine cell viability. Cell apoptosis was detected by a TUNEL assay and a flow cytometry cell apoptosis assay. Expression levels of proteins were measured by Western blotting. Intracellular calcium was assessed by Fura-2/AM staining. Flow cytometry was used to determine the mitochondrial membrane potential (MMP). Coimmunoprecipitation was used to evaluate the stability of the FKBP-RyR complex. Calcineurin enzymatic activity was measured with a colorimetric method. YAP nuclear translocation was tested by immunofluorescence staining. Results H/R induced HT-22 cell viability depression, and apoptosis was reversed by propofol treatment. Propofol could alleviate H/R-induced intracellular calcium accumulation and MMP loss by inhibiting calcineurin activity and FKBP12.6-RyR disassociation in a concentration-dependent manner. In addition, YAP expression was crucial for propofol to protect HT-22 cell apoptosis from H/R injury. Propofol could activate YAP through dephosphorylation. Activated YAP stimulated the transcription of the Bcl2 gene, which promotes cellular survival. Our data also demonstrated that propofol activated YAP through the RhoA-Lats1 pathway without large G proteins or MST involvement. In addition, we showed that there was no interaction between calcineurin signaling and YAP activation in HT-22 cells. Conclusions Propofol protected hippocampal neurons from I/R injury through two independent signaling pathways, including the calcineurin/FKBP12.6-RyR/calcium overload pathway and the RhoA/Lats1/YAP/Bcl-2 pathway.

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“…The adeno-associated virus (AAV) carrying RBM3 shRNA plasmid or empty plasmid was fused into CA3 region of hippocampus in mice two weeks before hypothermia in TBI mice. The image of green fluorescence showed that the adeno-associated virus carrying RBM3 shRNA plasmid or empty plasmid was delivered and expressed in CA3 (Figure 3A).Compared with TBI + HT + AAV-control group, the level of RBM3 in TBI + HT + shRNA-RBM3 group was significantly reduced in AAV injection region, suggesting that shRNA-RBM3 effectively blocks HT-induced RBM3 expression in TBI mice (Figure 3B-C).The previous and current studies have demonstrated that hypothermia reverses TBI-caused AD-like tau phosphorylation and brain dysfunction including impairment of LTP and spatial learning and memory 7,42. The ability of spatial learning and memory of all experimental mice isevaluated by Morris water maze.…”

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confidence: 77%

The overexpression of RBM3 alleviates TBI‐induced behaviour impairment and AD‐like tauopathy in mice

Liu

Cao

Shi

et al. 2020

J Cellular Molecular Medi

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Alzheimer disease (AD) is the most common form of dementia in older individuals and probably develops as a result of complex interactions among multiple factors, including age, genetics, environment, lifestyle and traumatic brain injury (TBI). 1-5 The evidence has shown that there appears to be a strong link between future risk of Alzheimer's and serious TBI, but how TBI increase future risk of AD is still unclear. 6-8 TBI caused by contact sports, work accident or military blasts may induce acute or potentially long-lasting neurological dysfunction, including chronic traumatic encephalopathy. 4-6,8,9 The clinical features of TBI vary depending on the mechanistic types and severity of head injury. These features generally consist of cognitive

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Downregulation of survivin regulates adult hippocampal neurogenesis and apoptosis, and inhibits spatial learning and memory following traumatic brain injury

Cited by 17 publications

References 42 publications

Lycium�barbarum polysaccharides protect human trophoblast HTR8/SVneo cells from hydrogen peroxide‑induced oxidative stress and apoptosis

Lycium�barbarum polysaccharides protect human trophoblast HTR8/SVneo cells from hydrogen peroxide‑induced oxidative stress and apoptosis

Propofol Protects Hippocampal Neurons from Hypoxia‐Reoxygenation Injury by Decreasing Calcineurin‐Induced Calcium Overload and Activating YAP Signaling

The overexpression of RBM3 alleviates TBI‐induced behaviour impairment and AD‐like tauopathy in mice

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