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ABSTRACT: ML355 rescued ALOX12 overexpression of cardiomyocytes after hypoxia-reoxygenation challenge

PROVIDER: PRJNA732247 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14630800.fastq.gz	Fastqsanger.gz
	SRR14630801.fastq.gz	Fastqsanger.gz
	SRR14630802.fastq.gz	Fastqsanger.gz
	SRR14630803.fastq.gz	Fastqsanger.gz
	SRR14630804.fastq.gz	Fastqsanger.gz

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Project description:RNA sequencing and subsequent bioinformatics analyses were performed at early reoxygenation stages in HL-1 cardiomyocytes treated or not with BRL37344 Methods: HL-1 cardiomyocytes were subjected to Hypoxia/Reoxygenation (6h/1h) with/without a M-NM-23AR agonist (BRL37344 5M-BM-5mol/L). mRNA profiles were generated by deep sequencing, in triplicate, using Illumina GAIIx.The sequence reads that passed quality filters were quantified using BWA aligned reads using RSEM. qRTM-bM-^@M-^SPCR validation was performed using SYBR Green assay. Results: After 6h of hypoxia followed by 1h reoxygenation, 866 genes were differentially expressed upon M-NM-23AR stimulation by BRL37344. Among these, 177 were at least 2-fold up or downregulated. Conclusions: Our results show that Hsp70 plays a key role in the cardioprotection afforded by M-NM-23AR agonism in cardiomyocytes during the early window of H/R. mRNA profiles from cardiomyocyte subjected to H/R (6h/1h) with/without a M-NM-23AR agonist were generated by deep sequencing, in triplicate, using Illumina GAIIx.

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Project description:RNA sequencing and subsequent bioinformatics analyses were performed at early reoxygenation stages in HL-1 cardiomyocytes treated or not with BRL37344 Methods: HL-1 cardiomyocytes were subjected to Hypoxia/Reoxygenation (6h/1h) with/without a β3AR agonist (BRL37344 5µmol/L). mRNA profiles were generated by deep sequencing, in triplicate, using Illumina GAIIx.The sequence reads that passed quality filters were quantified using BWA aligned reads using RSEM. qRT–PCR validation was performed using SYBR Green assay. Results: After 6h of hypoxia followed by 1h reoxygenation, 866 genes were differentially expressed upon β3AR stimulation by BRL37344. Among these, 177 were at least 2-fold up or downregulated. Conclusions: Our results show that Hsp70 plays a key role in the cardioprotection afforded by β3AR agonism in cardiomyocytes during the early window of H/R.

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Project description:Submergence induces hypoxia in plants; exposure to oxygen following submergence, termed reoxygenation, produces a burst of reactive oxygen species. The mechanisms of hypoxia sensing and signaling in plants have been well studied, but how plants respond to reoxygenation remains unclear. Here, we show that reoxygenation in Arabidopsis thaliana involves rapid accumulation of jasmonates (JAs) and increased transcript levels of JA biosynthesis genes. Application of exogenous methyl jasmonate improved tolerance to reoxygenation in wild-type Arabidopsis; also, mutants deficient in JA biosynthesis and signaling were very sensitive to reoxygenation. Moreover, overexpression of the transcription factor gene MYC2 enhanced tolerance to post-hypoxic stress and myc2 knockout mutants showed increased sensitivity to reoxygenation, indicating that MYC2 functions as a key regulator in the JA-mediated reoxygenation response. MYC2 transcriptionally activates members of the VITAMIN C DEFECTIVE (VTC) and GLUTATHIONE SYNTHETASE (GSH) gene families, which encode rate-limiting enzymes in the ascorbate and glutathione synthesis pathways. Overexpression of VTC1 and GSH1 in the myc2-2 mutant suppressed the post-hypoxic hypersensitive phenotype. The JA-inducible accumulation of antioxidants may alleviate oxidative damage caused by reoxygenation, improving plant survival after submergence. Taken together, our findings demonstrate that JA signaling interacts with the antioxidant pathway to regulate reoxygenation responses in Arabidopsis.

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Gene expression profiling in MCF7 cell lines under hypoxia and reoxygenation

Project description:Purpose: Study hypoxia and reoxygenation induced changes in genome-wide gene expression Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we performed a transcriptomics analysis in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia, reoxygenation). Results: Global downregulation upon hypoxia; partial restore on reoxygenation. Conclusions: Our data show that oxygen availability dynamically regulates gene transcription.

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