PMID- 36182869
OWN - NLM
STAT- MEDLINE
DCOM- 20221013
LR  - 20221222
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 631
DP  - 2022 Nov 26
TI  - The proatherosclerotic function of BCAT1 in atherosclerosis development of 
      aged-apolipoprotein E-deficient mice.
PG  - 93-101
LID - S0006-291X(22)01291-8 [pii]
LID - 10.1016/j.bbrc.2022.09.041 [doi]
AB  - Atherosclerosis (AS) is an inflammatory vascular disease. Branched-chain amino 
      acid transaminase 1 (BCAT1) has been implicated in inflammatory diseases, while 
      its role in AS is unclear yet. In ApoE(-/-) mice with a high fat diet (HDF), 
      BCAT1 was highly up-regulated and more pronounced in aged than in young ApoE(-/-) 
      mice, which was abundantly expressed in macrophages located in AS lesions. The 
      function of BCAT1 in AS was explored using lentivirus-mediated BCAT1 
      overexpression. ApoE(-/-) mice fed a HFD with BCAT1 overexpression exhibited the 
      worsening lipid deposition and pathological injury of aortic tissues, accompanied 
      by aggravated hyperlipidemia as proved by increased serum triglyceride, total 
      cholesterol, and low-density lipoprotein-cholesterol levels. Immunohistochemical 
      staining of vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant 
      protein-1 (MCP-1), and CD68 in the aortic root plaque suggested that BCAT1 
      overexpression could induce monocyte-endothelial cell adhesion and macrophages 
      infiltration, thereby contributing inflammatory response by promoting TNF-alpha, 
      IL-6, and IL-1beta expression. Further, in vivo experiments, lipid accumulation, and 
      inflammatory response induced by oxidized-LDL in RAW267.4 cells were also 
      intensified or alleviated by BCAT1 overexpression or knockdown. Finally, BCAT1 
      overexpression aggravated AS development. These adverse effects of BCAT1 on 
      hyperlipidemia, lipid accumulation, foaming cell formation, and inflammation 
      suggested that the modulation of BCAT1 might be a potential approach to prevent 
      AS disease.
CI  - Copyright (c) 2022 Elsevier Inc. All rights reserved.
FAU - Tan, Lili
AU  - Tan L
AD  - Department of Emergency Medicine, The Central Hospital Affiliated to Shenyang 
      Medical College, Shenyang, Liaoning, People's Republic of China. Electronic 
      address: tanlili123@163.com.
FAU - Lu, Jie
AU  - Lu J
AD  - Department of Cardiology, The Fourth People's Hospital of Shenyang, Shenyang, 
      Liaoning, People's Republic of China.
FAU - Zhang, Chunyang
AU  - Zhang C
AD  - Department of Emergency Medicine, The Central Hospital Affiliated to Shenyang 
      Medical College, Shenyang, Liaoning, People's Republic of China.
FAU - Meng, Liang
AU  - Meng L
AD  - Department of Cardiology, The Central Hospital Affiliated to Shenyang Medical 
      College, Shenyang, Liaoning, People's Republic of China.
FAU - Zhu, Qi
AU  - Zhu Q
AD  - Department of Emergency Medicine, The Central Hospital Affiliated to Shenyang 
      Medical College, Shenyang, Liaoning, People's Republic of China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220917
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Amino Acids, Branched-Chain)
RN  - 0 (Apolipoproteins E)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Triglycerides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - EC 2.6.1. (Bcat1 protein, mouse)
RN  - EC 2.6.1.- (Transaminases)
SB  - IM
MH  - Amino Acids, Branched-Chain
MH  - Animals
MH  - Apolipoproteins E/genetics
MH  - *Atherosclerosis/metabolism
MH  - Chemokine CCL2/metabolism
MH  - Cholesterol/metabolism
MH  - *Hyperlipidemias/genetics
MH  - Interleukin-6
MH  - Lipoproteins, LDL
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Transaminases/*metabolism
MH  - Triglycerides
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Vascular Cell Adhesion Molecule-1/metabolism
OTO - NOTNLM
OT  - Aged
OT  - Atherosclerosis
OT  - BCAT1
OT  - Inflammation
OT  - Lipid accumulation
OT  - Macrophages
COIS- Declaration of competing interest The authors have no conflicts of interest to 
      declare that are relevant to the content of this article.
EDAT- 2022/10/02 06:00
MHDA- 2022/10/14 06:00
CRDT- 2022/10/01 23:19
PHST- 2022/09/06 00:00 [received]
PHST- 2022/09/10 00:00 [accepted]
PHST- 2022/10/02 06:00 [pubmed]
PHST- 2022/10/14 06:00 [medline]
PHST- 2022/10/01 23:19 [entrez]
AID - S0006-291X(22)01291-8 [pii]
AID - 10.1016/j.bbrc.2022.09.041 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2022 Nov 26;631:93-101. doi: 
      10.1016/j.bbrc.2022.09.041. Epub 2022 Sep 17.