PMID- 33221374
OWN - NLM
STAT- MEDLINE
DCOM- 20211206
LR  - 20211214
IS  - 1873-3913 (Electronic)
IS  - 0898-6568 (Linking)
VI  - 78
DP  - 2021 Feb
TI  - HDAC1 promotes artery injury through activation of VAV3 by binding to miR-182-5p 
      in atherosclerotic mice model.
PG  - 109840
LID - S0898-6568(20)30317-X [pii]
LID - 10.1016/j.cellsig.2020.109840 [doi]
AB  - Atherosclerosis (AS) is one of the significant chronic inflammatory pathology 
      considering public health impact. Up-regulation of HDAC1 has been proved to be 
      related with endothelial dysfunction which is correlated intimately with AS. Our 
      research aims to investigate how histone deacetylase 1 (HDAC1)/miR-182-5p/vav 
      guanine nucleotide exchange factor 3 (VAV3)/AKT axis participates in AS in terms 
      of molecular mechanism. We detected miR-181-5p in human umbilical vein 
      endothelial cells after treatment with aorta and ox-LDL in AS model mice. Dual 
      luciferase reporter assay was employed to verify interaction of miR-182-5p and 
      VAV3. ChIP was performed to determine the relationship between HDAC1 and promoter 
      of miR-182-5p. Protein levels of HADC1, VAV3, AKT, p-AKT, vascular cell adhesion 
      molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and 
      monocyte chemotactic protein 1 (MCP-1) were detected by western blot analysis. 
      CCK8 and flow cytometry were used to detect cell viability and apoptosis, 
      respectively. After different treatments, the ability of cells to form monoclonal 
      cells was detected, and AS was evaluated by detecting arterial injury and 
      inflammation-related factors. Overexpression of HDAC1 could inhibit HUVECs 
      proliferation and promote AS in mouse model. It was verified by dual luciferase 
      assay that miR-182-5p could bind to VAV3 3'UTR mRNA. Meanwhile, HDAC1 repressed 
      miR-182-5p expression through binding to miR-182-5p promoter and then inhibit 
      VAV3 expression further. In summary, HDAC1 promoted AS through AKT pathway, which 
      was improved by VAV3 activation mediated by miR-182-5p. Our results demonstrated 
      that HDAC1 repressed miR-182-5p and activating AKT pathway via improving VAV3 to 
      promote AS progression.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Gao, Yanxia
AU  - Gao Y
AD  - Department of Emergency, The Second Affiliated Hospital of Xi'an Jiaotong 
      University, Xi'an 710004, PR China.
FAU - Pan, Longfei
AU  - Pan L
AD  - Department of Emergency, The Second Affiliated Hospital of Xi'an Jiaotong 
      University, Xi'an 710004, PR China.
FAU - Zhao, Li
AU  - Zhao L
AD  - Department of Emergency, The Second Affiliated Hospital of Xi'an Jiaotong 
      University, Xi'an 710004, PR China.
FAU - Dang, Xiaoyan
AU  - Dang X
AD  - Department of Emergency, The Second Affiliated Hospital of Xi'an Jiaotong 
      University, Xi'an 710004, PR China. Electronic address: dxiaoyan1@yeah.net.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201119
PL  - England
TA  - Cell Signal
JT  - Cellular signalling
JID - 8904683
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn182 microRNA, mouse)
RN  - 0 (Proto-Oncogene Proteins c-vav)
RN  - 0 (Vav3 protein, mouse)
RN  - EC 3.5.1.98 (Hdac1 protein, mouse)
RN  - EC 3.5.1.98 (Histone Deacetylase 1)
SB  - IM
MH  - Animals
MH  - *Aorta/injuries/metabolism
MH  - Atherosclerosis/genetics/*metabolism
MH  - Disease Models, Animal
MH  - Histone Deacetylase 1/genetics/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/metabolism
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Knockout, ApoE
MH  - MicroRNAs/genetics/*metabolism
MH  - Proto-Oncogene Proteins c-vav/genetics/*metabolism
MH  - *Signal Transduction
OTO - NOTNLM
OT  - AKT pathway
OT  - Aortic injury
OT  - Atherosclerosis
OT  - HDAC1
OT  - Inflammatory factor
OT  - MiR-182-5p
OT  - VAV3
EDAT- 2020/11/23 06:00
MHDA- 2021/12/15 06:00
CRDT- 2020/11/22 20:34
PHST- 2020/07/22 00:00 [received]
PHST- 2020/11/13 00:00 [revised]
PHST- 2020/11/13 00:00 [accepted]
PHST- 2020/11/23 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2020/11/22 20:34 [entrez]
AID - S0898-6568(20)30317-X [pii]
AID - 10.1016/j.cellsig.2020.109840 [doi]
PST - ppublish
SO  - Cell Signal. 2021 Feb;78:109840. doi: 10.1016/j.cellsig.2020.109840. Epub 2020 
      Nov 19.