Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery.
Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery.
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DOI:
10.1016/j.isci.2021.102305
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发表时间:
2021-04-23
期刊:
影响因子:
5.8
通讯作者:
Kurihara H
中科院分区:
文献类型:
--
作者:
Maruyama K;Naemura K;Arima Y;Uchijima Y;Nagao H;Yoshihara K;Singh MK;Uemura A;Matsuzaki F;Yoshida Y;Kurihara Y;Miyagawa-Tomita S;Kurihara H
Blood and lymphatic vessels surrounding the heart develop through orchestrated processes from cells of different origins. In particular, cells around the outflow tract which constitute a primordial transient vasculature, referred to as aortic subepicardial vessels, are crucial for the establishment of coronary artery stems and cardiac lymphatic vessels. Here, we revealed that the epicardium and pericardium-derived Semaphorin 3E (Sema3E) and its receptor, PlexinD1, play a role in the development of the coronary stem, as well as cardiac lymphatic vessels. In vitro analyses demonstrated that Sema3E may demarcate areas to repel PlexinD1-expressing lymphatic endothelial cells, resulting in proper coronary and lymphatic vessel formation. Furthermore, inactivation of Sema3E-PlexinD1 signaling improved the recovery of cardiac function by increasing reactive lymphangiogenesis in an adult mouse model of myocardial infarction. These findings may lead to therapeutic strategies that target Sema3E-PlexinD1 signaling in coronary artery diseases. Sema3E-PlexinD1 signaling regulates coronary and cardiac lymphatic vessel development Sema3E demarcate areas to repel PlexinD1-expressing lymphatic endothelial cells Inhibition of Sema3E-PlexinD1 signaling improves the recovery after myocardial injury Biological Sciences; Cell Biology; Developmental Biology
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