The pathological alterations in hearts from polycystic ovary syndrome mice [male_PAMH]
Polycystic ovary syndrome (PCOS), the most common endocrine disease in reproductive-aged women, is associated with an increased prevalence and extent of coronary artery disease. However, the underlying mechanism remains unclear. Here, we observed that hearts from PCOS mice were characterized by increased total macrophage accumulation. Monocyte-derived macrophages were significantly increased in the hearts of PCOS mice owing to enhanced circulating monocyte supply. Compared with control mice, PCOS mice showed a significant increase in splenic monocyte output, associated with elevated hematopoietic progenitors in the spleen and sympathetic tone. Compared with non-PCOS animals, PCOS-induced mice showed significantly exacerbated atherosclerotic plaque development and post-MI cardiac remodeling. Conditional Vcam1 silencing in PCOS mice significantly suppressed cardiac inflammation and improved post-MI cardiac injury. Our data documented new mechanisms through which PCOS may affect cardiovascular health in women. Overall design: Pregnant mice were treated with prenatal Anti-mullerian hormone (PAMH) treatment or PBS, and male offspring from each group were used for experiment. Then, we performed comparative gene expression profiling analysis of RNA-seq data for heart tissues from PAMH-treated male mice and control male mice.