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Effect of depletion of Anxa2 on gene expression during Oxygen-glucose deprivation and reoxygenation of BV2 microglia cells

ABSTRACT: Effect of depletion of Anxa2 on gene expression during Oxygen-glucose deprivation and reoxygenation of BV2 microglia cells

PROVIDER: PRJNA926665 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23195414_1.fastq.gz	Fastqsanger.gz
	SRR23195414_2.fastq.gz	Fastqsanger.gz
	SRR23195415_1.fastq.gz	Fastqsanger.gz
	SRR23195415_2.fastq.gz	Fastqsanger.gz
	SRR23195416_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of Anxa2 on gene expression during Oxygen-glucose deprivation and reoxygenation of BV2 microglia cells

Project description:To investigate the function Anxa2 in the regulation of immune inflammation after Oxygen-glucose deprivation and reoxygenation, we established BV2 microglia cells in Anxa2 has been knocked down by shRNA.

2024-02-10 | GSE223540 | GEO

Expression data from human astrocytes (HA) under oxygen-glucose deprivation / reoxygenation

Project description:Ischemia lead to neuronal injury. Dexmedetomidine and astrocytes are likely to protect neuronal cells against ischemia-induced injury. We used microarrays to examine the gene expression variation in astrocytes activated by oxygen-glucose deprivation and reoxygenation stress and identified distinct classes of genes up- and down-regulated by dexmedetomidine pretreatment.

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Expression data from human astrocytes (HA) under oxygen-glucose deprivation / reoxygenation

Project description:Expression data from human astrocytes (HA) under oxygen-glucose deprivation / reoxygenation

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Long non-coding RNA MALAT1 regulates angiogenesis following oxygen-glucose deprivation/reoxygenation.

Project description:Long non-coding RNAs (lncRNAs) have been identified as playing critical roles in multiple diseases. However, little is known regarding their roles and mechanisms in post-stroke angiogenesis. Our studies focused on deciphering the functional roles and the underlying mechanisms of the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in the process of angiogenesis following oxygen-glucose deprivation/reoxygenation (OGD/R). We characterized the up-regulation of MALAT1 expression in the process of angiogenesis after hypoxic injury in vivo and in vitro. We further showed that compared with the empty vector, MALAT1 knockdown had significantly reduced the capacity for angiogenesis, which was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT), scratching, cell cycle and immunofluorescent staining. Thus, our findings suggest that MALAT1 may mediate proangiogenic function in OGD/R. To further explore the potential mechanisms, we used lentiviruses expressing shMALAT1 and empty vector; the results revealed that shMALAT1 reduced the expression of 15-lipoxygenase 1 (15-LOX1), vascular endothelial growth factor (VEGF) and the phosphorylation of signal transducers and activators of transcription 3 (pSTAT3). Taken together, our results are the first to propose that MALAT1 may regulate angiogenesis through the 15-LOX1/STAT3 signalling pathway, and they may provide a critical target for the treatment of hypoxic injury and an avenue for therapeutic angiogenesis.

| S-EPMC6433728 | biostudies-literature

miRNA profile of microglial cells under oxygen-glucose deprivation

2015-11-23 | GSE63504 | GEO

Gene expression profile of microglial cells under oxygen-glucose deprivation

Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The mRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells.

2015-11-23 | GSE63505 | GEO

miRNA profile of microglial cells under oxygen-glucose deprivation

Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The miRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells. Two samples were analysed. miRNAs that were differentially expressed (increased or decreased in expression by â¥1.5-fold) between theOGD-activated and resting cells were identified.

2015-11-23 | E-GEOD-63504 | biostudies-arrayexpress

Ginsenoside Rh3 activates Nrf2 signaling and protects endometrial cells from oxygen and glucose deprivation-reoxygenation.

Project description:Oxygen and glucose deprivation (OGD)-reoxygenation (OGDR) induces oxidative injury to endometrial cells in vitro. We tested the potential effect of ginsenoside Rh3 (GRh3) in the process. Our results show that GRh3 activated Nrf2 signaling in T-HESC cells and primary murine endometrial cells. GRh3 induced Nrf2 Ser-40 phosphorylation and Keap1-Nrf2 disassociation, causing Nrf2 protein stabilization and nuclear translocation, which led to transcription and expression of antioxidant response element-dependent genes (HO1, NQO1 and GCLC). In T-HESC cells and primary murine endometrial cells, GRh3 potently attenuated OGDR-induced reactive oxygen species production, lipid peroxidation and mitochondrial depolarization, as well as cell viability reduction and necrosis. Activation of Nrf2 is required for GRh3-induced anti-OGDR actions in endometrial cells. Nrf2 inhibition, by Nrf2 shRNA, knockout (through CRISPR-Cas9-editing) or S40T mutation, abolished GRh3-induced endometrial cell protection against OGDR. Additionally, forced activation of Nrf2, by Keap1 knockout, mimicked and nullified GRh3-induced anti-OGDR actions in T-HESC cells. Together, we conclude that GRh3 protects endometrial cells from OGDR via activation of Nrf2 signaling.

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Project description:The miRNA-181 (miR-181) family regulates neuronal persistence during cerebral ischemia/reperfusion injury (CI/RI). Since the effect of miR-181d on CI/RI has never been studied, the current work sought to determine the involvement of miR-181d in neuronal apoptosis after brain I/R injury. To replicate in vivo and in vitro CI/RI, a transient middle cerebral artery occlusion (tMCAO) model in rats and an oxygen-glucose deficiency/reoxygenation (OGD/R) model in neuro 2A cells were developed. In both in vivo and in vitro stroke models, the expression of miR-181d was considerably higher. miR-181d suppression reduced apoptosis and oxidative stress in OGD/R-treated neuroblastoma cells, but miR-181d overexpression increased both. Furthermore, it was observed that miR-181d has a direct target in dedicator of cytokinesis 4 (DOCK4). The overexpression of DOCK4 partially overcame cell apoptosis and oxidative stress induced by miR-181d upregulation and OGD/R injury. Furthermore, the DOCK4 rs2074130 mutation was related to lower DOCK4 levels in ischemic stroke (IS) peripheral blood and higher susceptibility to IS. These findings suggest that downregulating miR-181d protects neurons from ischemic damage by targeting DOCK4, implying that the miR-181d/DOCK4 axis might be a novel therapeutic target for IS.

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Exosomal-miRNA sequencing of optineurin gene knockdown BV2 cells and wild type BV2 cells

Project description:To compare the miRNA profiles in exosomes derived from optineurin gene knockdown (Optn-KD)BV2s cells and wild type (WT) BV2 cells, BV2 cells were divided into two groups, Optn-KD group or WT group. We treated the Optn-KD group with Optn siRNA for 24 hours. Then, MiRNA profiles for each group were examined by Illumina HiSeq4000. We found differentiated miRNA profiles in the two groups. Compared with WT BV2 cell-derived exosomes, 4 miRNAs (miR-125b-5p, miR-351-5p, miR-505-5p, miR-novel-chr8_37700) were up-regulated and 2 miRNAs (miR-574-5p, miR-99b-5p) were down-regulated in Optn-KD BV2 cell-derived exosomes. This study provides a framework for characterizing the exosomal-miRNAs in Optn-KD BV2 cells.

2021-03-19 | GSE169175 | GEO

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