PMID- 19502284
OWN - NLM
STAT- MEDLINE
DCOM- 20091113
LR  - 20220321
IS  - 1755-3245 (Electronic)
IS  - 0008-6363 (Linking)
VI  - 84
IP  - 1
DP  - 2009 Oct 1
TI  - Regulatory T cells ameliorate hyperhomocysteinaemia-accelerated atherosclerosis 
      in apoE-/- mice.
PG  - 155-63
LID - 10.1093/cvr/cvp182 [doi]
AB  - AIMS: Atherosclerosis is an inflammatory disease with T cell-driven 
      immunoinflammatory responses contributing to disease initiation and progression. 
      We investigated the potential role of regulatory T cells (Tregs) in 
      hyperhomocysteinaemia (HHcy)-accelerated atherosclerosis in apoE-/- mice. METHODS 
      AND RESULTS: apoE-/- mice were fed normal mouse chow supplemented with or without 
      a high level of homocysteine (Hcy) (1.8 g/L) in drinking water for 2, 4, and 6 
      weeks. Atherosclerotic lesion area was slightly increased at 2 weeks and 
      substantially elevated at 4 and 6 weeks in HHcy apoE-/- mice. Cotransfer of 
      normal Tregs significantly attenuated atherosclerotic lesion size and 
      infiltration of T cells and macrophages into plaque. Furthermore, Treg cotransfer 
      reversed HHcy-accelerated proliferation of T cells, -increased pro-inflammatory, 
      and -decreased anti-inflammatory cytokine secretion from activated splenic T 
      cells. With a clinically relevant level of plasma Hcy, the proportion of Tregs 
      and suppressive activity in splenic T cells were reduced in HHcy apoE-/- mice, 
      which was associated with reduced mRNA and protein expression of Foxp3, a factor 
      governing mouse Treg development and function. In addition, Hcy significantly 
      attenuated the proportion and suppressive effects of Tregs in vitro. CONCLUSION: 
      HHcy suppresses the function of Tregs, which may be responsible for 
      HHcy-accelerated atherosclerosis in apoE-/- mice.
FAU - Feng, Juan
AU  - Feng J
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Science, 
      Peking University, Beijing 100191, PR China.
FAU - Zhang, Zhenmin
AU  - Zhang Z
FAU - Kong, Wei
AU  - Kong W
FAU - Liu, Bo
AU  - Liu B
FAU - Xu, Qingbo
AU  - Xu Q
FAU - Wang, Xian
AU  - Wang X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090605
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Apolipoproteins E)
RN  - 0 (Cytokines)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Foxp3 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Apolipoproteins E/*physiology
MH  - Atherosclerosis/etiology/*prevention & control
MH  - Cells, Cultured
MH  - Cytokines/biosynthesis
MH  - Female
MH  - Forkhead Transcription Factors/analysis/genetics
MH  - Hyperhomocysteinemia/*complications
MH  - Interleukin-10/physiology
MH  - Lymphocyte Activation
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - RNA, Messenger/analysis
MH  - T-Lymphocytes, Regulatory/*physiology
MH  - Transforming Growth Factor beta/physiology
EDAT- 2009/06/09 09:00
MHDA- 2009/11/17 06:00
CRDT- 2009/06/09 09:00
PHST- 2009/06/09 09:00 [entrez]
PHST- 2009/06/09 09:00 [pubmed]
PHST- 2009/11/17 06:00 [medline]
AID - cvp182 [pii]
AID - 10.1093/cvr/cvp182 [doi]
PST - ppublish
SO  - Cardiovasc Res. 2009 Oct 1;84(1):155-63. doi: 10.1093/cvr/cvp182. Epub 2009 Jun 
      5.