دورية أكاديمية
أعرض في EDS

c-JUN is a barrier in hESC to cardiomyocyte transition.

التفاصيل البيبلوغرافية
العنوان: c-JUN is a barrier in hESC to cardiomyocyte transition.
المؤلفون: Zhong H; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.; CAS Key Laboratory of Regenerative Biology, Center for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China., Zhang R; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.; https://ror.org/00zat6v61 Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.; Bioland Laboratory Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China., Li G; https://ror.org/00zat6v61 Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China., Huang P; The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, P.R. China., Zhang Y; Bioland Laboratory Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China., Zhu J; CAS Key Laboratory of Regenerative Biology, Center for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China., Kuang J; Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China., Hutchins AP; Department of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China., Qin D; https://ror.org/00zat6v61 Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China tanganqier@163.com.; Bioland Laboratory Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.; Centre for Regenerative Medicine and Health, Hong Kong Institute of Science & Innovation, Chinese Academy of Sciences; Hong Kong, China., Zhu P; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.; Guangdong Provincial Key Laboratory of Pathogenesis, Targeted Prevention and Treatment of Heart Disease and Guangzhou Key Laboratory of Pathogenesis, Targeted Prevention and Treatment of Heart Disease, Guangzhou, China., Pei D; Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China peiduanqing@westlake.edu.cn., Li D; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China lidongwei@gzhmu.edu.cn.; https://ror.org/00zat6v61 Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
المصدر: Life science alliance [Life Sci Alliance] 2023 Aug 21; Vol. 6 (11). Date of Electronic Publication: 2023 Aug 21 (Print Publication: 2023).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Life Science Alliance, LLC Country of Publication: United States NLM ID: 101728869 Publication Model: Electronic-Print Cited Medium: Internet ISSN: 2575-1077 (Electronic) Linking ISSN: 25751077 NLM ISO Abbreviation: Life Sci Alliance Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Woodbury, NY] : Life Science Alliance, LLC, [2018]-
مواضيع طبية MeSH: Human Embryonic Stem Cells* , Proto-Oncogene Proteins c-jun*/metabolism, Animals ; Humans ; Mice ; Cell Differentiation ; Chromatin/genetics ; Genes, jun ; Myocytes, Cardiac
مستخلص: Loss of c-JUN leads to early mouse embryonic death, possibly because of a failure to develop a normal cardiac system. How c-JUN regulates human cardiomyocyte cell fate remains unknown. Here, we used the in vitro differentiation of human pluripotent stem cells into cardiomyocytes to study the role of c-JUN. Surprisingly, the knockout of c-JUN improved cardiomyocyte generation, as determined by the number of TNNT2+ cells. ATAC-seq data showed that the c-JUN defect led to increased chromatin accessibility on critical regulatory elements related to cardiomyocyte development. ChIP-seq data showed that the knockout c-JUN increased RBBP5 and SETD1B expression, leading to improved H3K4me3 deposition on key genes that regulate cardiogenesis. The c-JUN KO phenotype could be copied using the histone demethylase inhibitor CPI-455, which also up-regulated H3K4me3 levels and increased cardiomyocyte generation. Single-cell RNA-seq data defined three cell branches, and knockout c-JUN activated more regulons that are related to cardiogenesis. In summary, our data demonstrated that c-JUN could regulate cardiomyocyte cell fate by modulating H3K4me3 modification and chromatin accessibility and shed light on how c-JUN regulates heart development in humans.
(© 2023 Zhong et al.)
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المشرفين على المادة: 0 (Chromatin)
0 (JUN protein, human)
0 (Proto-Oncogene Proteins c-jun)
تواريخ الأحداث: Date Created: 20230821 Date Completed: 20230828 Latest Revision: 20230830
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC10442936
DOI: 10.26508/lsa.202302121
PMID: 37604584
قاعدة البيانات: MEDLINE
الوصف
تدمد:2575-1077
DOI:10.26508/lsa.202302121