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Alterations in the expression of long noncoding RNAs and mRNAs in extracellular vesicles derived from the murine heart post ischemia-reperfusion injury

ABSTRACT: Alterations in the expression of long noncoding RNAs and mRNAs in extracellular vesicles derived from the murine heart post ischemia-reperfusion injury

PROVIDER: PRJNA784962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17074474_1.fastq.gz	Fastqsanger.gz
	SRR17074474_2.fastq.gz	Fastqsanger.gz
	SRR17074475_1.fastq.gz	Fastqsanger.gz
	SRR17074475_2.fastq.gz	Fastqsanger.gz
	SRR17074476_1.fastq.gz	Fastqsanger.gz

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Alterations in the expression of long noncoding RNAs and mRNAs in extracellular vesicles derived from the murine heart post ischemia-reperfusion injury

Project description:Extracellular vesicles (EVs) play important roles in cardiovascular diseases by delivering multiple RNA molecular, such as lncRNAs and mRNA. However, the features and functional mechanisms of the lncRNAs and mRNA in cardiac EVs during ischemia-reperfusion (IR) remains poorly understood. Therefore, we performed RNA sequencing to profile the expression feature of lncRNAs and mRNAs and predict their potential functions.

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Project description:Hepatic ischemia reperfusion injury is a dynamic process consisting of two stages: ischemia and reperfusion, and triggers a cascade of physiological and biochemical events. Given the important role of microRNAs in regulating gene expression, we analyzed gene expression changes in mouse livers at sham control, ischemia stage, and reperfusion stage. We generated global expression profiles of microRNA and mRNA genes in mouse livers subjected to ischemia reperfusion injury at the three stages, respectively. Comparison analysis showed that reperfusion injury had a distinct expression profile whereas the ischemia sample and the sham control were clustered together. Consistently, there are 69 differentially expressed microRNAs between the reperfusion sample and the sham control whereas 28 differentially expressed microRNAs between the ischemia sample and the sham control. We further identified two modes of microRNA expression changes in ischemia reperfusion injury. Functional analysis of both the differentially expressed microRNAs in the two modes and their target mRNAs revealed that ischemia injury impaired mitochondria function, nutrient consumption, and metabolism process. In contrast, reperfusion injury led to severe tissue inflammation that is predominantly an innate-immune response in the ischemia reperfusion process. Our staged analysis of gene expression profiles provides new insights into regulatory mechanisms of microRNAs in mouse hepatic ischemia reperfusion injury.

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Project description:Celastrol plays a significant role in cerebral ischemia-reperfusion injury. Although previous studies have confirmed that celastrol post-treatment has a protective effect on ischemic stroke, the therapeutic effect of celastrol on ischemic stroke and the underlying molecular mechanism remain unclear. In the present study, focal transient cerebral ischemia was induced by transient middle cerebral artery occlusion (tMCAO) in mice and celastrol was administered immediately after reperfusion. We performed lncRNA and mRNA analysis in the ischemic hemisphere of adult mice with celastrol post-treatment through RNA-Sequencing (RNA-Seq). A total of 50 differentially expressed lncRNAs (DE lncRNAs) and 696 differentially expressed mRNAs (DE mRNAs) were identified between the sham and tMCAO group, and a total of 544 DE lncRNAs and 324 DE mRNAs were identified between the tMCAO and tMCAO+celastrol group. Bioinformatic analysis was done on the identified deregulated genes through gene ontology (GO) analysis, KEGG pathway analysis and network analysis. Pathway analysis indicated that inflammation-related signaling pathways played vital roles in the treatment of ischemic stroke by celastrol. Our study suggests celastrol treatment can effectively reduce cerebral ischemia-reperfusion injury. The bioinformatics analysis of lnRNAs and mRNAs profiles in the ischemic hemisphere of adult mice provides a new perspective in the neuroprotective effects of celastrol, particularly with regards to ischemic stroke.

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