Abstract
BackgroundIn the clinic, variations in circadian rhythm are evident in patients with cardiovascular disease, and the risk of cardiovascular events increases when rhythms are disrupted. In this study, we focused on the role of the circadian gene period2 (per2) in mobilization and function of endothelial progenitor cells (EPCs) in vitro and in vivo after myocardial infarction (MI) in mice.Methods and ResultsMI was produced by surgical ligation of the left anterior descending coronary artery in mice with and without per2 deficiency. Trans-thoracic echocardiography was used to evaluate cardiac function in mice. Per2−/− mice with MI showed decreased cardiac function and increased infarct size. The number of CD34+ cells and capillary density were decreased in the myocardium of per2−/− mice on immunohistochemistry. Flow cytometry revealed decreased number of circulating EPCs in per2−/− mice after MI. In vitro, per2−/− EPCs showed decreased migration and tube formation capacity under hypoxia. Western blot analysis revealed inhibited activation of extracellular signal-regulated kinase and Akt signaling in the bone marrow of per2−/− mice and inhibited PI3K/Akt expression in per2−/− EPCs under hypoxia.ConclusionsPer2 modulates EPC mobilization and function after MI, which is important to recovery after MI in mice.
Highlights
For most of the past 2 decades, the role of the microvasculature in recovery from myocardial infarction (MI) has been considered important
Per2 modulates endothelial progenitor cells (EPCs) mobilization and function after MI, which is important to recovery after MI in mice
Per2 deficiency decreased the number of CD34+ cells and capillary density in the myocardium 4 weeks after MI
Summary
For most of the past 2 decades, the role of the microvasculature in recovery from myocardial infarction (MI) has been considered important. Studies of humans and animals have shown that a subpopulation of mononuclear cells with enhanced potential for differentiation into endothelial cells are mobilized endogenously from the bone marrow in response to MI and become incorporated into sites of new vessel growth in the ischemic tissue [1,2,3,4] These cells are known as endothelial progenitor cells (EPCs). Variations in circadian rhythm are evident in patients with cardiovascular diseases, and the risk of cardiovascular events increases when rhythms are disrupted [14,15,16,17]. Variations in circadian rhythm are evident in patients with cardiovascular disease, and the risk of cardiovascular events increases when rhythms are disrupted. We focused on the role of the circadian gene period (per2) in mobilization and function of endothelial progenitor cells (EPCs) in vitro and in vivo after myocardial infarction (MI) in mice
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