PMID- 26255138
OWN - NLM
STAT- MEDLINE
DCOM- 20160310
LR  - 20171116
IS  - 1165-158X (Electronic)
IS  - 0145-5680 (Linking)
VI  - 61
IP  - 3
DP  - 2015 Jul 31
TI  - Angiotensin II Promotes Atherogenesis through upregulating the Expression of 
      Connexin 43 in Dendritic Cells.
PG  - 96-101
AB  - It is known, for a long time, that angiotensin II (Ang II) could contribute to 
      atherogenesis (AS) and plaque vulnerability, however the underlying mechanisms 
      are poorly understood. Dendritic cells (DCs) are critical for the development of 
      both inflammation and atherogenesis. In the present study, we tried to 
      investigate the influence of AngII on the expression of connexin43 (Cx43) in DCs, 
      as well as the effect of AngII on AS. After mouse bone marrow—derived 
      dendritic cells (BMDCs) were treated by Ang II with or without Valsartan, the 
      expression of Cx43 was quantified by Western Blots. The expression of Cx43 and 
      CD40 (one marker of DCs) of DCs derived from AS plaques of ApoE—/— 
      mice was detected by immunohistochemistry double staining. The morphology of 
      atherosclerotic plaque was indicated by immunohistochemistry staining of smooth 
      muscle cells. The expression of Cx43 (P < 0.05) was increased significantly in 
      mouse BMDCs after treatment with AngII. In atherosclerotic plaques from 
      ApoE—/— mice expressing high levels of endogenous AngII, upregulation 
      of Cx43 (P < 0.01) and CD40 (P < 0.01) was observed. The upregulation and 
      pro—atherogenesis effect of Cx43 could be blocked by the AngII type 1 
      receptor blocker Valsartan, both in vitro and in vivo. AngII may promote 
      atherosclerosis and plaque vulnerability by increasing the expression of Cx43 in 
      DCs and inducing the maturation of DCs through the angiotensin II type 1 
      receptor.
FAU - Nie, W
AU  - Nie W
AD  - The First Affiliated Hospital of Zhejiang University, School of Medicine 
      Department of Cardiology Hangzhou China.
FAU - Yan, H
AU  - Yan H
AD  - The First Affiliated Hospital of Zhejiang University, School of Medicine 
      Department of Cardiology Hangzhou China.
FAU - Li, S
AU  - Li S
AD  - The First Affiliated Hospital of Zhejiang University, School of Medicine 
      Department of Cardiology Hangzhou China.
FAU - Zhu, W
AU  - Zhu W
AD  - The First Affiliated Hospital of Zhejiang University, School of Medicine 
      Department of Cardiology Hangzhou China.
FAU - Fan, F
AU  - Fan F
AD  - The First Affiliated Hospital of Zhejiang University, School of Medicine 
      Department of Cardiology Hangzhou China.
FAU - Zhu, J
AU  - Zhu J
AD  - The First Affiliated Hospital of Zhejiang University, School of Medicine 
      Department of Cardiology Hangzhou China zhujianhua2006@hotmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150731
PL  - France
TA  - Cell Mol Biol (Noisy-le-grand)
JT  - Cellular and molecular biology (Noisy-le-Grand, France)
JID - 9216789
RN  - 0 (Apolipoproteins E)
RN  - 0 (CD40 Antigens)
RN  - 0 (Connexin 43)
RN  - 0 (Lipopolysaccharides)
RN  - 11128-99-7 (Angiotensin II)
RN  - 80M03YXJ7I (Valsartan)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Animals
MH  - Apolipoproteins E/deficiency/genetics/metabolism
MH  - Atherosclerosis/*etiology
MH  - Blood Pressure/drug effects
MH  - CD40 Antigens/metabolism
MH  - Cells, Cultured
MH  - Connexin 43/genetics/*metabolism
MH  - Dendritic Cells/cytology/*drug effects/metabolism
MH  - Immunohistochemistry
MH  - Lipopolysaccharides/toxicity
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myocytes, Smooth Muscle/cytology/metabolism/pathology
MH  - Up-Regulation/*drug effects
MH  - Valsartan/pharmacology
EDAT- 2015/08/10 06:00
MHDA- 2016/03/11 06:00
CRDT- 2015/08/10 06:00
PHST- 2015/04/16 00:00 [received]
PHST- 2015/06/25 00:00 [accepted]
PHST- 2015/08/10 06:00 [entrez]
PHST- 2015/08/10 06:00 [pubmed]
PHST- 2016/03/11 06:00 [medline]
PST - epublish
SO  - Cell Mol Biol (Noisy-le-grand). 2015 Jul 31;61(3):96-101.