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Differential expression of cardiac mRNAs induced by Dexmedetomidine pretreatment in myocardial ischemia/reperfusion injury of mice

ABSTRACT: Differential expression of cardiac mRNAs induced by Dexmedetomidine pretreatment in myocardial ischemia/reperfusion injury of mice

PROVIDER: PRJNA867736 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22098042_1.fastq.gz	Fastqsanger.gz
	SRR22098042_2.fastq.gz	Fastqsanger.gz
	SRR22098043_1.fastq.gz	Fastqsanger.gz
	SRR22098043_2.fastq.gz	Fastqsanger.gz
	SRR22098044_1.fastq.gz	Fastqsanger.gz

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Differential expression of cardiac mRNAs induced by Dexmedetomidine pretreatment in myocardial ischemia/reperfusion injury of mice

Project description:To investigate the cardioprotection of Dexmedetomidine, we established myocardial ischemia/reperfusion models in mice with vehicle or Dexmedetomidine pretreatment. We then performed mRNA sequencing of cardiac tissues and conducted gene expression profiling analysis.

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Project description:Aims: Mesenchymal stem cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive. Strikingly, recent studies indicated that exosomes secreted by MSCs might be a novel mechanism for the beneficial effect of MSCs transplantation after myocardial infarction. We therefore explored the role of MSC-derived exosomes (MSC-Exo) in the immunomodulation of macrophages after myocardial ischemia-reperfusion and its implications in cardiac injury repair. Methods and Results: Exosomes were isolated from the supernatant of MSCs using a gradient centrifugation method. Administration of MSC-Exo through intramyocardial injection after myocardial ischemia reperfusion reduced infarct size and alleviated inflammation level in heart and serum. Systemic depletion of macrophages with clodronate liposomes abolished the curative effects of MSC-Exo. MSC-Exo modified the polarization of M1 macrophages to M2 macrophages both in vivo and in vitro. miRNA-sequencing of MSC-Exo and bioinformatics analysis implicated miR-182 as a potent candidate mediator of macrophage polarization and TLR4 as a downstream target. Diminishing miR-182 in MSC-Exo partially attenuated its modulation of macrophage polarization. Likewise, knock down of TLR4 also conferred cardioprotective efficacy and reduced inflammation level in a mouse model of myocardial ischemia/reperfusion. Conclusion: Our data indicates that MSC-Exo attenuates myocardial ischemia/reperfusion injury via shuttling miR-182 that modifies the polarization state of macrophages. This study sheds new light on the application of MSC-Exo a potential therapeutic tool for myocardial ischemia/reperfusion injury.

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