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Increased cardiac macrophages in Sorbs2-deficient hearts: revealing a potential role for macrophage in responding to embryonic myocardial abnormalities

ABSTRACT: Increased cardiac macrophages in Sorbs2-deficient hearts: revealing a potential role for macrophage in responding to embryonic myocardial abnormalities

PROVIDER: PRJNA1198960 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31735655_1.fastq.gz	Fastqsanger.gz
	SRR31735655_2.fastq.gz	Fastqsanger.gz
	SRR31735656_1.fastq.gz	Fastqsanger.gz
	SRR31735656_2.fastq.gz	Fastqsanger.gz
	SRR31735657_1.fastq.gz	Fastqsanger.gz

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Increased cardiac macrophages in Sorbs2-deficient hearts: revealing a potential role for macrophage in responding to embryonic myocardial abnormalities

Project description:Macrophages are known to support cardiac development and homeostasis, contributing to tissue remodeling and repair in the adult heart. However, it remains unclear whether embryonic macrophages also respond to abnormalities in the developing heart. Previously, we reported that the structural protein Sorbs2 promotes the development of the second heart field, with its deficiency resulting in atrial septal defects (ASD). In analyzing RNA-seq data, we noted an upregulation of macrophage-related genes in Sorbs2-/- hearts. Immunostaining and lineage-tracing confirmed an increase in macrophage numbers, underscoring a macrophage response to myocardial abnormalities. Partial depletion of macrophages led to downregulation of genes involved in lipid metabolism, muscle development and organ regeneration, alongside upregulation of genes associated with DNA damage-induced senescence and cardiomyopathy. Additionally, a non-significant increase in septal defects in macrophage-depleted Sorbs2-/- hearts suggests a potential reparative function for macrophages in maintaining structural integrity. Valve formation, however, remained unaffected. Our findings suggest that embryonic macrophages might sense abnormalities in embryonic cardiomyocytes and could adaptively support cardiac structure and function development in response to myocardial abnormalities.

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Project description:Chromosome 4q deletion syndrome is one of the most frequently detected genomic imbalance events in congenital heart disease (CHD) patients. However, a portion of terminal 4q deletions with CHD do not include known CHD genes. Here in a target sequencing of a panel of known and candidate CHD genes, we showed that the detrimental rare variants of SORBS2 in 4q35.1 are significantly enriched in CHD patients. Examination of Sorbs2-/- mouse hearts revealed two types of atrial septal defects (ASD), atrial hypoplasia/aplasia and double atrial septum. In vitro human cardiogenesis indicated a dual role of SORBS2 in maintaining sarcomeric integrity of cardiomyocytes and specifying the fate of cardiac progenitors. Mechanistically, SORBS2 promotes the commitment of the second heart field (SHF) over the first heart field (FHF) fate through c-ABL/NOTCH/SHH axis. Taken together, our data demonstrate that SORBS2 is a novel CHD gene within deleted 4q interval. The presence of double atrial septum in Sorbs2-/- mouse reveals the first molecular etiology of the rare anomaly linked to paradoxical thromboembolism.

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