KUDOVÁ, Jana, Ondřej VAŠÍČEK, Milan ČÍŽ and Lukáš KUBALA. Melatonin promotes cardiomyogenesis of embryonic stem cells via inhibition of HIF-1 alpha stabilization. JOURNAL OF PINEAL RESEARCH. HOBOKEN: WILEY, 2016, vol. 61, No 4, p. 493-503. ISSN 0742-3098. Available from: https://dx.doi.org/10.1111/jpi.12366.
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Basic information
Original name Melatonin promotes cardiomyogenesis of embryonic stem cells via inhibition of HIF-1 alpha stabilization
Authors KUDOVÁ, Jana (203 Czech Republic, belonging to the institution), Ondřej VAŠÍČEK (203 Czech Republic, belonging to the institution), Milan ČÍŽ (203 Czech Republic, belonging to the institution) and Lukáš KUBALA (203 Czech Republic, guarantor, belonging to the institution).
Edition JOURNAL OF PINEAL RESEARCH, HOBOKEN, WILEY, 2016, 0742-3098.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 10.391
RIV identification code RIV/00216224:14310/16:00097518
Organization unit Faculty of Science
Doi http://dx.doi.org/10.1111/jpi.12366
UT WoS 000386357100007
Keywords in English cardiomyogenesis; hypoxia-inducible factor-alpha; melatonin; mouse embryonic stem cells
Tags NZ, rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Radek Ševčík, Ph.D., učo 132566. Changed: 20/3/2018 12:59.
Abstract
Melatonin, a molecule involved in the regulation of circadian rhythms, has protective effects against myocardial injuries. However, its capability to regulate the maturation of cardiac progenitor cells is unclear. Recently, several studies have shown that melatonin inhibits the stabilization of hypoxia-inducible factors (HIFs), important signaling molecules with cardioprotective effects. In this study, by employing differentiating mouse embryonic stem cells, we report that melatonin significantly upregulated the expression of cardiac cell-specific markers (myosin heavy chains six and seven) as well as the percentage of myosin heavy chain-positive cells. Importantly, melatonin decreased HIF-1 alpha stabilization and transcriptional activity and, in contrast, induced HIF-2 alpha stabilization. Interestingly, the deletion of HIF-1 alpha completely inhibited the pro-cardiomyogenic effect of melatonin as well as the melatonin-mediated HIF-2 alpha stabilization. Moreover, melatonin increased Sirt-1 levels in a HIF-1 alpha-dependent manner. Taken together, we provide new evidence of a time-specific inhibition of HIF-1 alpha stabilization as an essential feature of melatonin-induced cardiomyogenesis and unexpected different roles of HIF-1 alpha stabilization during various stages of cardiac development. These results uncover new mechanisms underlying the maturation of cardiac progenitor cells and can help in the development of novel strategies for using melatonin in cardiac regeneration therapy.
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