Comprehensive epigenome characterization reveals diverse transcriptional regulation across human vascular endothelial cells.


Journal

Epigenetics & chromatin
ISSN: 1756-8935
Titre abrégé: Epigenetics Chromatin
Pays: England
ID NLM: 101471619

Informations de publication

Date de publication:
19 12 2019
Historique:
received: 14 08 2019
accepted: 03 12 2019
entrez: 21 12 2019
pubmed: 21 12 2019
medline: 27 5 2020
Statut: epublish

Résumé

Endothelial cells (ECs) make up the innermost layer throughout the entire vasculature. Their phenotypes and physiological functions are initially regulated by developmental signals and extracellular stimuli. The underlying molecular mechanisms responsible for the diverse phenotypes of ECs from different organs are not well understood. To characterize the transcriptomic and epigenomic landscape in the vascular system, we cataloged gene expression and active histone marks in nine types of human ECs (generating 148 genome-wide datasets) and carried out a comprehensive analysis with chromatin interaction data. We developed a robust procedure for comparative epigenome analysis that circumvents variations at the level of the individual and technical noise derived from sample preparation under various conditions. Through this approach, we identified 3765 EC-specific enhancers, some of which were associated with disease-associated genetic variations. We also identified various candidate marker genes for each EC type. We found that the nine EC types can be divided into two subgroups, corresponding to those with upper-body origins and lower-body origins, based on their epigenomic landscape. Epigenomic variations were highly correlated with gene expression patterns, but also provided unique information. Most of the deferentially expressed genes and enhancers were cooperatively enriched in more than one EC type, suggesting that the distinct combinations of multiple genes play key roles in the diverse phenotypes across EC types. Notably, many homeobox genes were differentially expressed across EC types, and their expression was correlated with the relative position of each organ in the body. This reflects the developmental origins of ECs and their roles in angiogenesis, vasculogenesis and wound healing. This comprehensive analysis of epigenome characterization of EC types reveals diverse transcriptional regulation across human vascular systems. These datasets provide a valuable resource for understanding the vascular system and associated diseases.

Sections du résumé

BACKGROUND
Endothelial cells (ECs) make up the innermost layer throughout the entire vasculature. Their phenotypes and physiological functions are initially regulated by developmental signals and extracellular stimuli. The underlying molecular mechanisms responsible for the diverse phenotypes of ECs from different organs are not well understood.
RESULTS
To characterize the transcriptomic and epigenomic landscape in the vascular system, we cataloged gene expression and active histone marks in nine types of human ECs (generating 148 genome-wide datasets) and carried out a comprehensive analysis with chromatin interaction data. We developed a robust procedure for comparative epigenome analysis that circumvents variations at the level of the individual and technical noise derived from sample preparation under various conditions. Through this approach, we identified 3765 EC-specific enhancers, some of which were associated with disease-associated genetic variations. We also identified various candidate marker genes for each EC type. We found that the nine EC types can be divided into two subgroups, corresponding to those with upper-body origins and lower-body origins, based on their epigenomic landscape. Epigenomic variations were highly correlated with gene expression patterns, but also provided unique information. Most of the deferentially expressed genes and enhancers were cooperatively enriched in more than one EC type, suggesting that the distinct combinations of multiple genes play key roles in the diverse phenotypes across EC types. Notably, many homeobox genes were differentially expressed across EC types, and their expression was correlated with the relative position of each organ in the body. This reflects the developmental origins of ECs and their roles in angiogenesis, vasculogenesis and wound healing.
CONCLUSIONS
This comprehensive analysis of epigenome characterization of EC types reveals diverse transcriptional regulation across human vascular systems. These datasets provide a valuable resource for understanding the vascular system and associated diseases.

Identifiants

pubmed: 31856914
doi: 10.1186/s13072-019-0319-0
pii: 10.1186/s13072-019-0319-0
pmc: PMC6921469
doi:

Substances chimiques

Chromatin 0
Histones 0
Homeodomain Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

77

Subventions

Organisme : Japan Agency for Medical Research and Development
ID : JP16gm0510005h0006
Pays : International
Organisme : Japan Agency for Medical Research and Development
ID : JP19am0101105
Pays : International
Organisme : Japan Society for the Promotion of Science
ID : 17H06331
Pays : International
Organisme : Japan Society for the Promotion of Science
ID : JP18H05527
Pays : International

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Auteurs

Ryuichiro Nakato (R)

Laboratory of Computational Genomics, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, 113-0032, Japan.
Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.

Youichiro Wada (Y)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan. ywada-tky@umin.ac.jp.
Isotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan. ywada-tky@umin.ac.jp.

Ryo Nakaki (R)

Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Genta Nagae (G)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Yuki Katou (Y)

Laboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, 113-0032, Japan.

Shuichi Tsutsumi (S)

Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Natsu Nakajima (N)

Laboratory of Computational Genomics, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, 113-0032, Japan.

Hiroshi Fukuhara (H)

Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.

Atsushi Iguchi (A)

Department of Cardiovascular Surgery, Saitama Medical University International Medical Center, Saitama, 350-1298, Japan.

Takahide Kohro (T)

Department of Clinical Informatics, Jichi Medical University School of Medicine, Shimotsuke, 329-0498, Japan.

Yasuharu Kanki (Y)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Isotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan.

Yutaka Saito (Y)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Artificial Intelligence Research Center, National Institute of Advanced Industrial Science and Technology (AIST), 2-4-7 Aomi, Koto-ku, Tokyo, 135-0064, Japan.
Computational Bio Big-Data Open Innovation Laboratory (CBBD-OIL), National Institute of Advanced Industrial Science and Technology (AIST), 3-4-1 Okubo, Shinjuku-ku, Tokyo, 169-8555, Japan.

Mika Kobayashi (M)

Isotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan.

Akashi Izumi-Taguchi (A)

Isotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan.

Naoki Osato (N)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Kenji Tatsuno (K)

Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Asuka Kamio (A)

Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Yoko Hayashi-Takanaka (Y)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, 226-8503, Japan.

Hiromi Wada (H)

Isotope Science Center, The University of Tokyo, Tokyo, 113-0032, Japan.
Brain Attack Center, Ohta Memorial Hospital, Fukuyama, 720-0825, Japan.

Shinzo Ohta (S)

Brain Attack Center, Ohta Memorial Hospital, Fukuyama, 720-0825, Japan.

Masanori Aikawa (M)

The Center for Excellence in Vascular Biology and the Center for Interdisciplinary Cardiovascular Sciences, Cardiovascular Division and Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.

Hiroyuki Nakajima (H)

Department of Cardiovascular Surgery, Saitama Medical University International Medical Center, Saitama, 350-1298, Japan.

Masaki Nakamura (M)

Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.

Rebecca C McGee (RC)

Lifeline Cell Technology, Frederick, MD, 21701, USA.

Kyle W Heppner (KW)

Lifeline Cell Technology, Frederick, MD, 21701, USA.

Tatsuo Kawakatsu (T)

Bio-Medical Department, Kurabo Industries Ltd., Neyagawa, Osaka, 572-0823, Japan.

Michiru Genno (M)

Bio-Medical Department, Kurabo Industries Ltd., Neyagawa, Osaka, 572-0823, Japan.

Hiroshi Yanase (H)

Bio-Medical Department, Kurabo Industries Ltd., Neyagawa, Osaka, 572-0823, Japan.

Haruki Kume (H)

Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.

Takaaki Senbonmatsu (T)

Department of Cardiology, Saitama Medical University International Medical Center, Saitama, 350-1298, Japan.

Yukio Homma (Y)

Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.

Shigeyuki Nishimura (S)

Department of Cardiology, Saitama Medical University International Medical Center, Saitama, 350-1298, Japan.

Toutai Mitsuyama (T)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Artificial Intelligence Research Center, National Institute of Advanced Industrial Science and Technology (AIST), 2-4-7 Aomi, Koto-ku, Tokyo, 135-0064, Japan.

Hiroyuki Aburatani (H)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan.
Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.

Hiroshi Kimura (H)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan. hkimura@bio.titech.ac.jp.
Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, 226-8503, Japan. hkimura@bio.titech.ac.jp.
Laboratory of Functional Nuclear Imaging, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, 113-0032, Japan. hkimura@bio.titech.ac.jp.

Katsuhiko Shirahige (K)

Japan Agency for Medical Research and Development (AMED-CREST), AMED, 1-7-1 Otemachi, Chiyoda-ku, Tokyo, 100-0004, Japan. kshirahi@iam.u-tokyo.ac.jp.
Laboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, 113-0032, Japan. kshirahi@iam.u-tokyo.ac.jp.

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