期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 13, 页码 -出版社
MDPI
DOI: 10.3390/ijms22137015
关键词
bioactive lipids; biomolecules; cardiac injury; cardiac differentiation; cardiomyocyte differentiation; cardiogenic transcription factors
资金
- National Research Foundation of Korea (NRF) [2017M3A9B3061830, 2017R1A5A2015395]
- National Research Foundation of Korea (NRF) of the Ministry of Science, ICT and Future Planning, Korea
- National Research Foundation of Korea [2017R1A5A2015395] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
This study identified O-cyclic phytosphingosine-1-phosphate (cP1P) as a novel factor that significantly enhances the differentiation potential of human embryonic stem cells (hESCs) into cardiomyocytes. Treatment with cP1P was found to increase the beating colony number and contracting area of cardiomyocytes. Furthermore, the molecular mechanism of cP1P regulating SMAD1/5/8 signaling via the ALK3/BMP receptor cascade during cardiac differentiation was elucidated. The results provide a new insight for using cP1P to improve the quality of cardiomyocyte differentiation for regenerative therapies.
Adult human cardiomyocytes have an extremely limited proliferative capacity, which poses a great barrier to regenerative medicine and research. Human embryonic stem cells (hESCs) have been proposed as an alternative source to generate large numbers of clinical grade cardiomyocytes (CMs) that can have potential therapeutic applications to treat cardiac diseases. Previous studies have shown that bioactive lipids are involved in diverse cellular responses including cardiogenesis. In this study, we explored the novel function of the chemically synthesized bioactive lipid O-cyclic phytosphingosine-1-phosphate (cP1P) as an inducer of cardiac differentiation. Here, we identified cP1P as a novel factor that significantly enhances the differentiation potential of hESCs into cardiomyocytes. Treatment with cP1P augments the beating colony number and contracting area of CMs. Furthermore, we elucidated the molecular mechanism of cP1P regulating SMAD1/5/8 signaling via the ALK3/BMP receptor cascade during cardiac differentiation. Our result provides a new insight for cP1P usage to improve the quality of CM differentiation for regenerative therapies.
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