Nature Communications (Aug 2020)
Epsin-mediated degradation of IP3R1 fuels atherosclerosis
- Yunzhou Dong,
- Yang Lee,
- Kui Cui,
- Ming He,
- Beibei Wang,
- Sudarshan Bhattacharjee,
- Bo Zhu,
- Tadayuki Yago,
- Kun Zhang,
- Lin Deng,
- Kunfu Ouyang,
- Aiyun Wen,
- Douglas B. Cowan,
- Kai Song,
- Lili Yu,
- Megan L. Brophy,
- Xiaolei Liu,
- Jill Wylie-Sears,
- Hao Wu,
- Scott Wong,
- Guanglin Cui,
- Yusuke Kawashima,
- Hiroyuki Matsumoto,
- Yoshio Kodera,
- Richard J. H. Wojcikiewicz,
- Sanjay Srivastava,
- Joyce Bischoff,
- Da-Zhi Wang,
- Klaus Ley,
- Hong Chen
Affiliations
- Yunzhou Dong
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Yang Lee
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Kui Cui
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Ming He
- Department of Medicine, University of California, San Diego
- Beibei Wang
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Sudarshan Bhattacharjee
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Bo Zhu
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Tadayuki Yago
- Cardiovascular Biology Program, Oklahoma Medical Research Foundation
- Kun Zhang
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Lin Deng
- Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School
- Kunfu Ouyang
- Department of Medicine, University of California, San Diego
- Aiyun Wen
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Douglas B. Cowan
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Kai Song
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Lili Yu
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Megan L. Brophy
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Xiaolei Liu
- Center for Vascular and Developmental Biology, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine
- Jill Wylie-Sears
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Hao Wu
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Scott Wong
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Guanglin Cui
- Department of Nutrition and Epidemiology, Harvard T.H. Chan School of Public Health
- Yusuke Kawashima
- Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center
- Hiroyuki Matsumoto
- Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center
- Yoshio Kodera
- Center for Disease Proteomics, Kitasato University School of Science
- Richard J. H. Wojcikiewicz
- Department of Pharmacology, SUNY Upstate Medical University
- Sanjay Srivastava
- Department of Medicine, Division of Cardiovascular Medicine, University of Louisville School of Medicine
- Joyce Bischoff
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Da-Zhi Wang
- Department of Cardiology, Boston Children’s Hospital, Harvard Medical School
- Klaus Ley
- La Jolla Institute for Allergy and Immunology
- Hong Chen
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- DOI
- https://doi.org/10.1038/s41467-020-17848-4
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 16
Abstract
Endothelial cell (EC) dysfunction and inflammation contribute to plaque destabilization in atherosclerosis, increasing the risk of thrombotic events. Here, the authors show that epsin promotes EC inflammation via a mechanism involving IP3R1 degradation, and that deletion of epsin in the endothelium prevents EC dysfunctoin and atherosclerosis in mice.
