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Cardio-immune Interaction via a Clusterin-TLR4 Axis Suppresses Inflammation and Triggers Regeneration

ABSTRACT: This study aimed to investigate the transcriptional effects of BMP2 treatment on neonatal mouse cardiomyocytes. Primary cardiomyocytes were treated with either PBS or BMP2 and subjected to bulk RNA sequencing to profile BMP2-induced changes in gene expression. To further dissect the underlying signaling mechanisms, cells were co-treated with the BMP2 receptor inhibitor Dorsomorphin, allowing assessment of the contribution of the canonical SMAD pathway to BMP2-mediated transcriptional regulation. Comparative transcriptomic analysis across treatment groups provides new insights into the role of the BMP2–SMAD signaling axis in cardiomyocyte gene regulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE307310 | GEO | 2025/11/24

REPOSITORIES: GEO

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Project description:To compare expression profiles in the cardiomyocytes with wild type top2b and those with top2b deletion after in vivo treatment of mice with doxorubicin or drug vehicle Doxorubicin is widely used in modern cancer treatments, despite the advent of targeted therapy. However, a dose-dependent cardiotoxicity often limits its clinical use. The prevailing theory hypothesizes that doxorubicin-induced cardiotoxicity is the result of reactive oxygen species (ROS) generation due to redox-cycling of doxorubicin. Here we showed that cardiomyocyte-specific deletion of Topoisomerase II beta (Top2b) markedly reduced DNA double-strand breaks, apoptosis, and functional damages in doxorubicin-treated hearts. To investigate transcriptomic changes after doxorubicin treatment in wild type mouse and mouse with cardiac specific deletion of Top2b, we examined the expression profiles in 4 groups of mice (3/group), ie. wildtype mice with or without doxorubicin treatment and mice with Top2b deletion in the cardiomyocytes with or without doxorubicin treatment. Mice were treated with doxorubicin (25mg/kg, i.p.) or PBS (drug vehicle) for 16 hr or 72 hr. The heart was removed and cardiomyocytes were isolated by using a Langendorff apparatus. After purification, total RNA was extracted from the cardiomyocytes, purified, and used for gene expression analysis. Compared with that in control cardiomyocytes or cardiomyocytes with Top2b deletion, doxorubicin caused a significant expression change in the genome of cardiomyocytes from the wildtype mice. Among the changes, multiple genes encoding mitochondrial structural protein and components of the respiratory chain complexes were down-regulated 72 hr after treatment while multiple genes in the p53 pathway were up-regulated 16 hr after treatment in the wildtype cardiomyocytes. Expression changes were examined in 2 groups of mice (wild type and conditional knockout of top2b in the cardiomyocytes) treated with doxorubicin or PBS for 16 or 72 hours

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Cardio-immune Interaction via a Clusterin-TLR4 Axis Suppresses Inflammation and Triggers Regeneration

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