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Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [bulk RNA-seq]

ABSTRACT: Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [bulk RNA-seq]

PROVIDER: PRJNA1098021 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28597871_1.fastq.gz	Fastqsanger.gz
	SRR28597871_2.fastq.gz	Fastqsanger.gz
	SRR28597872_1.fastq.gz	Fastqsanger.gz
	SRR28597872_2.fastq.gz	Fastqsanger.gz
	SRR28597873_1.fastq.gz	Fastqsanger.gz

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Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [scRNA-seq]

Project description:Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [scRNA-seq]

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Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [scRNA-seq]

Project description:Cardiac macrophages are heterogenous in phenotype and functions, which has been associated with differences in their ontogeny. Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. We here investigated macrophage lineages and ablated tissue macrophages in homeostasis and after I/R injury in a CSF1R-dependent manner. Genomic deletion of a fms-intronic regulatory element (FIRE) in the Csf1r locus resulted in specific absence of resident homeostatic and antigen-presenting macrophages, without affecting the recruitment of monocyte-derived macrophages to the infarcted heart. Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. In contrast, continuous CSF1R inhibition led to depletion of both resident and recruited macrophage populations. This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. These findings attribute distinct beneficial effects to different macrophage populations in the context of myocardial infarction.

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Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [bulk RNA-seq]

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LncRNA and mRNA profiling of the ischemia zone, the border zone and the remote non-ischemia zone of murine myocardial ischemia/reperfusion (MI/R) hearts

Project description:Purpose：Detection of differentially expressed lncRNA in the infarct zone and the control group in myocardial ischemia-reperfusion injury model tissue. Method: Use 8 weeks of C57BL/6 mice to establish a myocardial ischemia-reperfusion injury model, 45 minutes of ischemia, and 24 hours after reperfusion, the mice were sacrificed to obtain materials. Result: The expression of lncRNAs in the infarct area of myocardial ischemia-reperfusion injury model mice was detected, and it was found that a total of 43 lncRNAs related to myocardial ischemia-reperfusion injury changed in expression, of which 17 were up-regulated (fold change >1.5). 26 expressions are down-regulated (fold change <0.8)

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Project description:Background–Acute coronary syndrome (ACS) is sometimes accompanied by accelerated coagulability, lipid metabolism, and inflammatory responses, which are not attributable to the cardiac events alone. We hypothesized that the liver plays a pivotal role in the pathophysiology of ACS. We simultaneously analyzed the gene expression profiles of the liver and heart during acute myocardial ischemia in mice. Methods and Results–Mice were divided into three treatment groups: sham-operation, ischemia-reperfusion (I/R), and myocardial infarction. Mice with liver I/R were included as additional controls. Marked changes in hepatic gene expression were observed after 24 hours, despite the lack of histological changes in the liver. Genes related to tissue remodeling, adhesion molecules, and morphogenesis were significantly upregulated in the livers of mice with myocardial I/R or infarction, but not in those with liver I/R. Myocardial ischemia, but not changes in the hemodynamic state, was postulated to significantly alter hepatic gene expression. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver. To address these points, we utilized isolated primary hepatocytes and showed that osteopontin released from the heart actually altered the signaling pathways of primary hepatocytes to those observed in the livers of mice under myocardial ischemia. Moreover, osteopontin stimulated primary hepatocytes to secrete vascular endothelial growth factor-A, which is important for tissue remodeling. Conclusions– Hepatic gene expression is potentially regulated by cardiac humoral factors under myocardial ischemia. These results provide new insights into the pathophysiology of ACS.

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