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Transcriptomic study of the HT22 cells after OGD treatment.

ABSTRACT: Transcriptomic study of the HT22 cells after OGD treatment.

PROVIDER: PRJNA741816 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14925900_1.fastq.gz	Fastqsanger.gz
	SRR14925900_2.fastq.gz	Fastqsanger.gz
	SRR14925901_1.fastq.gz	Fastqsanger.gz
	SRR14925901_2.fastq.gz	Fastqsanger.gz
	SRR14925902_1.fastq.gz	Fastqsanger.gz

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Transcriptomic study of the HT22 cells after OGD treatment.

Project description:To investigate the key genes of ischemic stroke, the oxygen glucose deprivation model and RNA sequence of HT22 neuronal cells were performed. By comparing with each other, we identified 51 up-regulated and 119 down-regulated genes in 3H vs 0H, 229 up-regulated and 50 down-regulated genes in 6H-vs-3H, and 145 up-regulated and 121 down-regulated genes in 6H-vs-0H. The results indicate that c-Fos acts as the most key gene at 51 up-regulated genes in 3H vs 0H.

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChipM-BM-. Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour. The gene expression profile from the J147-treated HT22 cells (1 hour exposure) was compared to HT22 cells treated with vehicle only (DMSO) for 1 hour. The DMSO/vehicle treated cells serve as the control and are referred to as untreated with drug.

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChip® Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour.

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Global transcriptomic profiling of oxygen-glucose deprivation (OGD)-mediated neuronal injury

Project description:Oxygen-glucose deprivation (OGD) is a cellular phenomenon consistently observed upon occurrence of ischemic stroke which eventually results in neuronal death. Neuronal cell death after ischemia takes place via two distinct processes, necrosis and apoptosis. Apoptosis, programmed cell death, is denoted by chromatin condensation, nuclear blebbing, cellular shrinkage, and DNA fragmentation. Unlike apoptosis, cellular swelling and lysis is suggestive of necrosis. However, these two processes are related not only to the severity but also to the duration of ischemia. Microarray analysis was carried out using 20 Illumina mouse Ref8V1.1 genechip arrays. The assignment of the arrays was as follows: Controls (n=5); exposure to OGD for 10min, 5h, 8h, 15h and 24 h (n=3 respectively).

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The mRNAs alteration induced by Neat1 knockdown in HT22 cells

Project description:We knocked down the lncRNA-Neat1 by RNA interference in HT22 cells, which were immortalized from the mice hippocampal neurons. Then we measured the mRNA alteration induced by Neat1 knockdown through the next generation sequencing technique (RNA-seq). A total of 18,309 transcripts were detected in the current sequencing study, in which 593 transcripts were selected out according to the criteria: |log2(fold change)| > 1, P < 0.05 (22 up-regulated and 571 down-regulated). To explore whether the mRNA change induced by Neat1 knockdown in a stressed culture condition was different from that in normal condition, the cells were dealt with OGD and followed by RNA-seq. A total of 18,502 transcripts were detected, in which 121 transcripts were significantly up-regulated and 126 transcripts were significantly down-regulated according to the aforementioned filter rules.

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The mRNA alteration in HT22 cells induced by the overexpression of long noncoding RNA AK046375

Project description:We overexpressed the lncRNA-AK046375 by lentivirus in HT22 cells, which were immortalized from the mice hippocampal neurons. Then we measured the mRNA alteration induced by AK046375 overexpression through the next generation sequencing technique (RNA-seq). A total of 20,319 transcripts were detected in the current sequencing study, in which 1342 transcripts were selected out according to the criteria: |log2(fold change)| > 1, P < 0.05 (717 up-regulated and 625 down-regulated). To explore whether the mRNA change induced by AK046375 overexpression in a stressed culture condition was different from that in normal condition, the cells were dealt with oxygen-glucose-deprived(OGD) and followed by RNA-seq. A total of 22,016 transcripts were detected, in which 87 transcripts were significantly up-regulated and 131 transcripts were significantly down-regulated according to the aforementioned filter rules.

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Identification of Klf9-regulated genes in HT22 tissue culture cells [RNA-Seq]

Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration. We used mouse hippocampus-derived HT22 cell line to identify genes differentially regulated by forced Klf9 expression. We stably transfected HT22 cells with pCDNA6:TR (encoding the Tet repressor) and pCDNA6:TO-Klf9 (encoding Klf9 downstream of the Tet operator), allowing doxycycline(dox)-inducible expression of Klf9. We chose a stably transfected clone with baseline Klf9 mRNA level similar to that of untransfected HT22 cells (parent line) and approximately 10-fold induction after dox treatment. We conducted RNA-seq on stably transfected HT22 cells treated with or without dox for 8 hours; we also conducted RNA-seq on parent cells subjected to the same dox treatment to separate nonspecific effects of dox from the effects of forced Klf9 expression. Analysis of RNA-seq data found 217 gene repressed and 21 upregulated by forced Klf9 expression (FDR-adjusted p<.005; because fold changes were small we used a stringent p value cutoff to ensure that we were studying genes likely to be bona fide targets), showing that Klf9 functions primarily as a transcriptional repressor. Gene ontology analysis showed that Klf9-repressed genes were enriched in cytoskeletal and Wnt signaling-related genes.

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