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Cardiac Mesenchymal Cells from Failing Hearts Limit Ventricular Dilation when Administered Late after Infarction

ABSTRACT: Cardiac Mesenchymal Cells from Failing Hearts Limit Ventricular Dilation when Administered Late after Infarction

PROVIDER: PRJNA602494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10919415_1.fastq.gz	Fastqsanger.gz
	SRR10919415_2.fastq.gz	Fastqsanger.gz
	SRR10919416_1.fastq.gz	Fastqsanger.gz
	SRR10919416_2.fastq.gz	Fastqsanger.gz
	SRR10919417_1.fastq.gz	Fastqsanger.gz

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Project description:Background: Cardiac macrophages have been implicated in myocardial repair following myocardial infarction (MI), yet their therapeutic potential in ischemic cardiomyopathy (ICM) remains limited by an incomplete understanding of their molecular regulation. CD163 is highly expressed in these macrophages, yet its functional role in regulating post-MI cardiac repair remains unknown. Methods: A cross-sectional clinical study was conducted to assess the association between circulating soluble CD163 concentration and heart failure due to ICM. To investigate the functional contribution of CD163 in ICM, Wild-type (WT) and Cd163/ mice were subjected to permanent ligation of the left anterior descending coronary artery. Single-cell RNA sequencing was employed to analyze transcriptional changes in cardiac immune cells. Recombinant osteopontin (OPN) and CD163 were administered to assess their therapeutic effect in Cd163/ mice. Results: Circulating soluble CD163 levels were markedly elevated in patients with ICM-induced heart failure compared with individuals without heart failure (median difference 34.5 ng/mL, IQR 13.6–54.6 ng/mL, P = 0.002) and showed a positive correlation with the extent of systolic dysfunction and left ventricular dilation. Cd163/ mice displayed aggravated left ventricular systolic dysfunction, reduced ejection fraction and fractional shortening, impaired myocardial strain, and reduced relative wall thickness post-MI. Recombinant CD163 protein could reverse systolic dysfunction and left ventricular dilation in Cd163/ mice after MI. CD163 was predominantly expressed in CCR2⁻ resident cardiac macrophages, and CD163 deficiency altered transcriptional programs of macrophages without affecting their polarization status, with enrichment in cytokine signaling and extracellular matrix-related pathways. Spp1 (OPN) expression was significantly downregulated in Cd163/ hearts under both sham and MI conditions. Administration of recombinant OPN improved systolic function, reduced ventricular dilation, decreased fibrotic scar size, and restored the elastin-to-collagen ratio in Cd163/ mice. Conclusions: In cardiac macrophages, CD163 contributes to post-myocardial infarction repair by upregulating OPN expression, which in turn helps maintain systolic function.

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Cardiac Mesenchymal Cells from Failing Hearts Limit Ventricular Dilation when Administered Late after Infarction

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