PMID- 27782101
OWN - NLM
STAT- MEDLINE
DCOM- 20170505
LR  - 20190606
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 22
DP  - 2016 Oct 26
TI  - Angiotensin II Promotes the Development of Carotid Atherosclerosis in Type 2 
      Diabetes Patients via Regulating the T Cells Activities: A Cohort Study.
PG  - 4000-4008
AB  - BACKGROUND Specific T cell phenotype has been reported to potentially contribute 
      to the development of angiotensin II (Ang II)-induced several vascular disorders. 
      Type 2 diabetes mellitus (T2DM) is intimately associated with cardiovascular 
      disease. The present study aimed to investigate the relationship between T cell 
      phenotypes and Ang II in T2DM patients combined with carotid atherosclerosis 
      (CA). MATERIAL AND METHODS This study was performed on 50 patients with T2DM in 
      our hospital. Based on the presence of CA, they were divided into CA group 
      (presence of CA, n=30) or T2DM group (absence of CA, n=20). Additionally, 10 
      healthy participants were selected as controls. Basic characteristics of all 
      participants were collected and recorded. Peripheral blood mononuclear cells 
      (PBMCs) isolated from patients and controls with or without Ang II and Ang II 
      receptor blocker (ARB) treatment were used to detect Th1, Th2, and Th17 cell 
      proportions, mRNA levels of T-bet, GATA3, and RORgammat as well as the expression of 
      IFN-gamma, IL-4, and IL-17 by flow cytometry, ELISA, and Real-Time PCR. RESULTS Ang 
      II levels were notably higher in patients in the CA group than those in the T2DM 
      and control group (p<0.05). Th1 and Th17 positive cells, mRNA levels of T-bet and 
      RORgt as well as the expression of IFN-gamma and IL-17 were significantly increased 
      in the CA group compared with the T2DM group and control group (p<0.05). 
      Moreover, the activities of T cells and related cytokines were significantly 
      increased of healthy controls after Ang II treatment (p<0.05), while these 
      changes were notably weakened by ARB treatment (p<0.05). CONCLUSIONS Ang II 
      promotes the development of CA in T2DM patients by regulating T cells activities.
FAU - Wang, Kai
AU  - Wang K
AD  - Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical 
      University, Chongqing, China (mainland).
FAU - Jin, Feng
AU  - Jin F
AD  - Department of Radiology, The Affiliated Hospital of Inner Mongolia Medical 
      University, Hohhot, Inner Mongolia, China (mainland).
FAU - Zhang, Zhanpu
AU  - Zhang Z
AD  - Department of Neurosurgery, The Affiliated Hospital of Inner Mongolia Medical 
      University, Hohhot, Inner Mongolia, China (mainland).
FAU - Sun, Xiaochuan
AU  - Sun X
AD  - Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical 
      University, Chongqing, China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20161026
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Cytokines)
RN  - 11128-99-7 (Angiotensin II)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Angiotensin II/*immunology
MH  - Carotid Artery Diseases/*immunology/pathology
MH  - Cohort Studies
MH  - Cytokines/metabolism
MH  - Diabetes Mellitus, Type 2/*immunology/pathology
MH  - Female
MH  - Humans
MH  - Leukocytes, Mononuclear/immunology/pathology
MH  - Lymphocyte Activation/immunology
MH  - Male
MH  - Middle Aged
MH  - Phenotype
MH  - T-Lymphocyte Subsets/immunology
MH  - T-Lymphocytes/*immunology/pathology
PMC - PMC5094472
COIS- Conflict interests The authors declared that there is no conflict of interest.
EDAT- 2016/10/27 06:00
MHDA- 2017/05/06 06:00
PMCR- 2016/10/26
CRDT- 2016/10/27 06:00
PHST- 2016/10/27 06:00 [pubmed]
PHST- 2017/05/06 06:00 [medline]
PHST- 2016/10/27 06:00 [entrez]
PHST- 2016/10/26 00:00 [pmc-release]
AID - 900842 [pii]
AID - 10.12659/msm.900842 [doi]
PST - epublish
SO  - Med Sci Monit. 2016 Oct 26;22:4000-4008. doi: 10.12659/msm.900842.