PMID- 35990936
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220823
IS  - 2297-055X (Print)
IS  - 2297-055X (Electronic)
IS  - 2297-055X (Linking)
VI  - 9
DP  - 2022
TI  - YB1 dephosphorylation attenuates atherosclerosis by promoting CCL2 mRNA decay.
PG  - 945557
LID - 10.3389/fcvm.2022.945557 [doi]
LID - 945557
AB  - Chronic inflammation is a key pathological process in atherosclerosis. RNA 
      binding proteins (RBPs) have been reported to play an important role in 
      atherosclerotic plaque formation, and they could regulate the expression of 
      inflammatory factors by phosphorylation modification. Y-box binding protein 1 
      (YB1) is an RBP that has participated in many inflammatory diseases. Here, we 
      found an increased expression of phosphorylated YB1 (pYB1) in atherosclerotic 
      plaques and demonstrated that YB1 dephosphorylation reduced lipid accumulation 
      and lesion area in the aorta in vivo. Additionally, we found that inflammatory 
      cytokines were downregulated in the presence of YB1 dephosphorylation, 
      particularly CCL2, which participates in the pathogenesis of atherosclerosis. 
      Furthermore, we demonstrated that CCL2 mRNA rapid degradation was mediated by the 
      glucocorticoid receptor-mediated mRNA decay (GMD) process during YB1 
      dephosphorylation, which resulted in the downregulation of CCL2 expression. In 
      conclusion, YB1 phosphorylation affects the development of atherosclerosis 
      through modulating inflammation, and targeting YB1 phosphorylation could be a 
      potential strategy for the treatment of atherosclerosis by anti-inflammation.
CI  - Copyright (c) 2022 Tang, Li, Yang, Yang, Geng, Liu, Zhang, Liu, Xue, Zhang, Wang 
      and Zhao.
FAU - Tang, Yaqin
AU  - Tang Y
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Li, Zhiwei
AU  - Li Z
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Yang, Hongqin
AU  - Yang H
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Yang, Yang
AU  - Yang Y
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Geng, Chi
AU  - Geng C
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Liu, Bin
AU  - Liu B
AD  - Jilin Zhongtai Biotechnology Co., Ltd, Jilin, China.
FAU - Zhang, Tiantian
AU  - Zhang T
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Liu, Siyang
AU  - Liu S
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Xue, Yunfei
AU  - Xue Y
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Zhang, Hongkai
AU  - Zhang H
AD  - The Pathology Department, Beijing Hospital of Traditional Chinese Medicine, The 
      Capital Medical University, Beijing, China.
FAU - Wang, Jing
AU  - Wang J
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
FAU - Zhao, Hongmei
AU  - Zhao H
AD  - State Key Laboratory of Medical Molecular Biology, Department of Pathophysiology, 
      Peking Union Medical College, Institute of Basic Medical Sciences, Chinese 
      Academy of Medical Sciences, Beijing, China.
LA  - eng
PT  - Journal Article
DEP - 20220804
PL  - Switzerland
TA  - Front Cardiovasc Med
JT  - Frontiers in cardiovascular medicine
JID - 101653388
PMC - PMC9386362
OTO - NOTNLM
OT  - RNA binding protein
OT  - atherosclerosis
OT  - inflammation
OT  - mRNA decay
OT  - phosphorylation
COIS- Author BL was employed by the company Jilin Zhongtai Biotechnology. The remaining 
      authors declare that the research was conducted in the absence of any commercial 
      or financial relationships that could be construed as a potential conflict of 
      interest.
EDAT- 2022/08/23 06:00
MHDA- 2022/08/23 06:01
PMCR- 2022/01/01
CRDT- 2022/08/22 04:03
PHST- 2022/05/16 00:00 [received]
PHST- 2022/07/14 00:00 [accepted]
PHST- 2022/08/22 04:03 [entrez]
PHST- 2022/08/23 06:00 [pubmed]
PHST- 2022/08/23 06:01 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 10.3389/fcvm.2022.945557 [doi]
PST - epublish
SO  - Front Cardiovasc Med. 2022 Aug 4;9:945557. doi: 10.3389/fcvm.2022.945557. 
      eCollection 2022.