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Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [heart]

ABSTRACT: Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [heart]

PROVIDER: PRJNA1030930 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26463701.fastq.gz	Fastqsanger.gz
	SRR26463702.fastq.gz	Fastqsanger.gz
	SRR26463703.fastq.gz	Fastqsanger.gz
	SRR26463704.fastq.gz	Fastqsanger.gz

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Project description:Purpose:to verify Drp1-mediated biological pathways under physiological and ischemia conditions.Methods:C57BL/6 mice and Drp1 knockdown mice were used for ischemia treatment. Right femoral arteries were catheterized with polyethylene catheters for bleeding 50% of total blood volume (≈7% of weight). The ischemia time started to calculate after the model was established. A laparotomy was then carried out to obtain superior mesenteric artery tissues (SMAs) for transcriptome analysis. Series-Cluster analysis was performed to identify the global trends of mitochondrial DEGs after Drp1 knockdown. Gene ontology (GO) analysis was performed to facilitate elucidating the biological process (BP), molecular function (MF) and cellular component (CC) of unique genes in the significant or representative profiles. Results:In addition to its traditional roles in GTPase regulation and mitochondrial fission, Drp1 may also regulate actin cytoskeleton and the movement of microtubules. Besides, Drp1 may participate in the regulation of morphology and functions of other organelles, including endoplasmic reticulum, peroxisome, phagolysosome, etc. As for general organ functions, Drp1 may regulate vascular constriction and dilation. These consequences indicated the important role of Drp1 in ischemia-induced cellular regulation. Conclusions: Drp1 deficiency proves the important role of Drp1 in ischemia-induced biomedical processes through multiple potential fission-independent manners. Methods:C57BL/6 mice and Drp1 knockdown mice were used for ischemia treatment. Right femoral arteries were catheterized with polyethylene catheters for bleeding 50% of total blood volume (≈7% of weight). The ischemia time started to calculate after the model was established. A laparotomy was then carried out to obtain superior mesenteric artery tissues (SMAs) for transcriptome analysis. Series-Cluster analysis was performed to identify the global trends of mitochondrial DEGs after Drp1 knockdown. Gene ontology (GO) analysis was performed to facilitate elucidating the biological process (BP), molecular function (MF) and cellular component (CC) of unique genes in the significant or representative profiles. Results:In addition to its traditional roles in GTPase regulation and mitochondrial fission, Drp1 may also regulate actin cytoskeleton and the movement of microtubules. Besides, Drp1 may participate in the regulation of morphology and functions of other organelles, including endoplasmic reticulum, peroxisome, phagolysosome, etc. As for general organ functions, Drp1 may regulate vascular constriction and dilation. These consequences indicated the important role of Drp1 in ischemia-induced cellular regulation. Conclusions: Drp1 deficiency proves the important role of Drp1 in ischemia-induced biomedical processes through multiple potential fission-independent manners.

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Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [heart]

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