MicroRNA-34b mediates hippocampal astrocyte apoptosis in a rat model of recurrent seizures

Liu, Liqun; Shi, Jiayun; Tan, Menglin; Xiong, Jie; Li, Xing‐Fang; Hu, Qing-peng; Yi, Zhu-Wen; Mao, Ding-An

doi:10.1186/s12868-016-0291-6

Cited by 28 publications

(27 citation statements)

References 45 publications

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“…Prostaglandins such as PGD2 and PGE2 have been revealed to exacerbate hypoxic injury in neurons [30]. Moreover, several miRs have recently been reported to be associated with hypoxia and ischemia [31, 32] and to have protective roles in neuron damage, such as miR-34b-5p expression in astrocytes [33] and miR-210 downregulation of glucocorticoid receptor protein, and in the neonatal brain in response to HIBD [9]. Importantly, the miR-592 level has also been reported to decrease after cerebral ischemia, and miR-592 overexpression decreases ischemic injuries in neurons [34].…”

Section: Discussionmentioning

confidence: 99%

Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

Sun

Guo

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study aimed to explore the effect of microRNA-592-5p (miR-592-5p) on hypoxic-ischemic brain damage (HIBD)-induced hippocampal neuronal injury in a neonatal mouse model relative to the involvement of one target gene, PTGDR, and the PGD2/ DP signaling pathway. Methods: A total of 30 neonatal mice aged 7 days were randomly selected to establish an HIBD mouse model. Hippocampal neuronal cells were transfected into a control group, a blank group, a negative control (NC) group, an miR-592-5p mimics group, an miR-592-5p inhibitors group, an siRNA-PTGDR group and an miR-592-5p inhibitors + siRNA-PTGDR group. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot analyses were performed to detect the expression levels of miR-592-5p, PTGDR, DP2, Bcl-2 and Bax in tissues and cells. Cell proliferation, cell cycle and apoptosis were detected by MTT assay and flow cytometry, respectively. Results: The expression levels of miR-592-5p and Bcl-2 decreased, while the expression levels of PTGDR, DP2 and Bax increased in the HIBD group. PTGDR is a target gene of miR-592-2p. Compared with the NC and blank groups, the expression levels of PTGDR, DP2 and Bax decreased, while the expression levels of miR-592-5p and Bcl-2 increased in the miR-592-5p mimics group. The siRNA-PTGDR group showed the same trend as that observed in the miR-592-5p mimics group, except with no difference in miR-592-5p expression. The miR-592-5p inhibitors group showed an opposite gene expression trend compared to that in the miR-592-5p mimics group. The S phase of the cell cycle was prolonged, the G1 phase was reduced, proliferation was increased, and the apoptosis rate was decreased in the siRNA-PTGDR and miR-592-5p mimics groups. Opposite trends for cell cycle, proliferation and apoptosis were observed in the miR-592-5p inhibitors group. Conclusions: Our study suggests that miR-592-5p upregulation protects against hippocampal neuronal injury caused by HIBD by targeting PTGDR and inhibiting the PGD2/DP signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

Sun

Guo

Zhang

et al. 2018

Cell Physiol Biochem

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“…It was reported that up‐regulation of the nuclear factor of kappa B (NF‐κB) pathway can promote anti‐apoptosis of cells under oxidative stress . Bcl‐2 protein has been thought of as an anti‐apoptotic protein . Therefore, we evaluated the anti‐apoptotic effect of NF‐κB pathway activation in MSCs under oxidative stress, with Bcl‐2 as an indicator.…”

Section: Introductionmentioning

confidence: 99%

TNF‐α promotes survival and migration of MSCs under oxidative stress via NF‐κB pathway to attenuate intimal hyperplasia in vein grafts

Bai

et al. 2017

J Cellular Molecular Medi

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The oxidative stress caused by endothelial injury is involved in intimal hyperplasia (IH) in vein grafts. Mesenchymal stem cells (MSCs) can home to injured intima and promote endothelial repair. However, MSC apoptosis is increased accompanied by decreased functional activity under oxidative stress. Thus, we investigate whether tumour necrosis factor‐α (TNF‐α) can promote the survival and activity of MSCs under oxidative stress to reduce IH more effectively, and establish what role the NF‐κB pathway plays in this. In this study, we preconditioned MSCs with TNF‐α (TNF ‐α‐PCMSCs) for 24 hrs and measured the activation of the IKK/NF‐κB pathway. EdU and transwell assays were performed to assess proliferation and migration of TNF ‐α‐PCMSCs. Apoptosis and migration of TNF ‐α‐ PCMSCs were evaluated in conditions of oxidative stress by analysis of the expression of Bcl‐2 and CXCR4 proteins. TNF ‐α‐ PCMSCs were transplanted into a vein graft model, so that cell homing could be tracked, and endothelial apoptosis and IH of vein grafts were measured. The results demonstrated that TNF‐α promotes proliferation and migration of MSCs. Furthermore, survival and migration of TNF ‐α‐ PCMSCs under oxidative stress were both enhanced. A greater number of MSCs migrated to the intima of vein grafts after preconditioning with TNF‐α, and the formation of neointima was significantly reduced. These effects could be partially abolished by IKK XII (NF‐κB inhibitor). All these results indicate that preconditioning with TNF‐α can promote survival and migration of MSCs under oxidative stress via the NF‐κB pathway and thus attenuate IH of vein grafts.

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“…The single miR reported changed in four studies, miR-34b, was increased in all four, suggesting it may play an important role. Mir-34b is interesting as it plays a role in brain development [92] and in Parkinson’s disease [93] as well as regulating apoptosis of astrocytes in the setting of seizures [94]. Of 79 miRNAs reported changed in two studies, 44% reported the same direction of change (increased or decreased) in both.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Changes in Preconditioning-Induced Neuroprotection

Bell

Cho

Giffard

2017

Transl. Stroke Res.

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Preconditioning is a paradigm in which sub-lethal stress – prior to a more injurious insult – induces protection against injury. In the central nervous system (CNS), preconditioning against ischemic stroke is induced by short durations of ischemia, brief seizures, exposure to anesthetics, and other stresses. Increasing evidence supports the contribution of microRNAs (miRNAs) to the pathogenesis of cerebral ischemia and ischemic tolerance induced by preconditioning. Studies investigating miRNA changes induced by preconditioning have to date identified 562 miRNAs that change expression levels after preconditioning, and 15% of these changes were reproduced in at least one additional study. Of miRNAs assessed as changed by preconditioning in more than one study, about 40% changed in the same direction in more than one study. Most of the studies to assess the role of specific miRNAs in the neuroprotective mechanism of preconditioning were performed in vitro, with fewer studies manipulating individual miRNAs in vivo. Thus, while many miRNAs change in response to preconditioning stimuli, the mechanisms underlying their effects are not well understood. The data does suggest that miRNAs may play significant roles in preconditioning-induced neuroprotection. This review focuses on the current state of knowledge of the possible role of miRNAs in preconditioning-induced cerebral protection.

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MicroRNA-34b mediates hippocampal astrocyte apoptosis in a rat model of recurrent seizures

Cited by 28 publications

References 45 publications

Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

TNF‐α promotes survival and migration of MSCs under oxidative stress via NF‐κB pathway to attenuate intimal hyperplasia in vein grafts

MicroRNA Changes in Preconditioning-Induced Neuroprotection

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