PMID- 28848136
OWN - NLM
STAT- MEDLINE
DCOM- 20171116
LR  - 20190212
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 42
IP  - 6
DP  - 2017
TI  - Mir-22-3p Inhibits Arterial Smooth Muscle Cell Proliferation and Migration and 
      Neointimal Hyperplasia by Targeting HMGB1 in Arteriosclerosis Obliterans.
PG  - 2492-2506
LID - 10.1159/000480212 [doi]
AB  - BACKGROUND: Aberrant vascular smooth muscle cell (VSMC) proliferation and 
      migration contribute to the development of vascular pathologies, such as 
      atherosclerosis and post-angioplasty restenosis. The aim of this study was to 
      determine whether miR-22-3p plays a role in regulating human artery vascular 
      smooth muscle cell (HASMC) function and neointima formation. METHODS: 
      Quantitative real-time PCR (qRT-PCR) and fluorescence in situ hybridization 
      (FISH) were used to detect miR-22-3p expression in human arteries. Cell Counting 
      Kit-8 (CCK-8) and EdU assays were performed to assess cell proliferation, and 
      transwell and wound closure assays were performed to assess cell migration. 
      Moreover, luciferase reporter assays were performed to identify the target genes 
      of miR-22-3p. Finally, a rat carotid artery balloon-injury model was used to 
      determine the role of miR-22-3p in neointima formation. RESULTS: MiR-22-3p 
      expression was downregulated in arteriosclerosis obliterans (ASO) arteries 
      compared with normal arteries, as well as in platelet-derived growth factor-BB 
      (PDGF-BB)-stimulated HASMCs compared with control cells. MiR-22-3p overexpression 
      had anti-proliferative and anti-migratory effects and dual-luciferase assay 
      showed that high mobility group box-1 (HMGB1) is a direct target of miR-22-3p in 
      HASMCs. Furthermore, miR-22-3p expression was negatively correlated with HMGB1 
      expression in ASO tissue specimens. Finally, LV-miR-22-3p-mediated miR-22-3p 
      upregulation significantly suppressed neointimal hyperplasia specifically by 
      reducing HMGB1 expression in vivo. CONCLUSIONS: Our results indicate that 
      miR-22-3p is a key molecule in regulating HASMC proliferation and migration by 
      targeting HMGB1 and that miR-22-3p and HMGB1 may be therapeutic targets in the 
      treatment of human ASO.
CI  - (c) 2017 The Author(s). Published by S. Karger AG, Basel.
FAU - Huang, Shui-Chuan
AU  - Huang SC
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
AD  - Department of Vascular Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
FAU - Wang, Mian
AU  - Wang M
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
FAU - Wu, Wei-Bin
AU  - Wu WB
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
FAU - Wang, Rui
AU  - Wang R
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
FAU - Cui, Jin
AU  - Cui J
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
FAU - Li, Wen
AU  - Li W
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
FAU - Li, Zi-Lun
AU  - Li ZL
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
FAU - Li, Wen
AU  - Li W
AD  - Laboratory of General Surgery, First Affiliated Hospital, Sun Yat-sen University, 
      Guangzhou, China.
AD  - Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, 
      Guangzhou, China.
AD  - Vascular Surgical Disease Research Center of Guangdong Province, Guangzhou, 
      China.
FAU - Wang, Shen-Ming
AU  - Wang SM
AD  - Department of Vascular Surgery, First Affiliated Hospital, Sun Yat-Sen 
      University, Guangzhou, China.
AD  - Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, 
      Guangzhou, China.
AD  - Vascular Surgical Disease Research Center of Guangdong Province, Guangzhou, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20170822
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Antagomirs)
RN  - 0 (HMGB1 Protein)
RN  - 0 (MicroRNAs)
RN  - 0 (Proto-Oncogene Proteins c-sis)
RN  - 1B56C968OA (Becaplermin)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Animals
MH  - Antagomirs/metabolism
MH  - Arteriosclerosis Obliterans/metabolism/*pathology
MH  - Base Sequence
MH  - Becaplermin
MH  - Carotid Artery Injuries/metabolism/pathology/veterinary
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - HMGB1 Protein/antagonists & inhibitors/genetics/*metabolism
MH  - Humans
MH  - Male
MH  - MicroRNAs/antagonists & inhibitors/genetics/*metabolism
MH  - Muscle, Smooth, Vascular/cytology/drug effects/metabolism
MH  - Proto-Oncogene Proteins c-sis/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sequence Alignment
OTO - NOTNLM
OT  - Arteriosclerosis
OT  - HMGB1
OT  - Human arterial smooth muscle cell
OT  - Migration
OT  - Mirna-22-3p
OT  - Neointimal hyperplasia
OT  - Proliferation
EDAT- 2017/08/30 06:00
MHDA- 2017/11/29 06:00
CRDT- 2017/08/30 06:00
PHST- 2017/03/23 00:00 [received]
PHST- 2017/06/15 00:00 [accepted]
PHST- 2017/08/30 06:00 [pubmed]
PHST- 2017/11/29 06:00 [medline]
PHST- 2017/08/30 06:00 [entrez]
AID - 000480212 [pii]
AID - 10.1159/000480212 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2017;42(6):2492-2506. doi: 10.1159/000480212. Epub 2017 Aug 
      22.