PMID- 28849148
OWN - NLM
STAT- MEDLINE
DCOM- 20180607
LR  - 20240314
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 16
IP  - 5
DP  - 2017 Nov
TI  - Subcutaneous injection of dendritic cells aggravates atherosclerosis in 
      ApoE‑knockout mice by activation of TLR4.
PG  - 6041-6049
LID - 10.3892/mmr.2017.7339 [doi]
AB  - Dendritic cells (DCs) are specialized antigen‑presenting cells which are 
      important in immune diseases, in particular atherosclerosis, a chronic 
      inflammatory disease, however their role in atherosclerosis‑associated immunity 
      is unclear. To evaluate the role of DCs in atherosclerosis, exogenous bone 
      marrow‑derived DCs were transferred into ApoE‑/‑ mice in the present study. The 
      extent of disease was measured in the aorta and was compared with mice treated 
      with phosphate‑buffered saline (PBS) or left untreated and fed a western diet. 
      Mice receiving exogenous DCs demonstrated significantly larger atherosclerotic 
      lesions compared with the mice treated with PBS, with increasing numbers of 
      mature DCs in circulation and enhanced DC infiltration into plaque lesions, in 
      addition to activation of circulating inflammatory components and atherosclerotic 
      lesions. Furthermore, it was demonstrated that exogenous DCs upregulated the 
      expression of Toll‑like receptor 4 (TLR4) on DCs, which may be an important 
      mechanism to activate DCs and aggravate atherosclerosis. Therefore the present 
      study concluded that exogenous DCs may induce maturation of endogenous DCs via 
      upregulation of TLR4, further increasing the inflammatory response and 
      accelerating atherosclerosis.
FAU - Ye, Zhishuai
AU  - Ye Z
AD  - Department of Cardiology, The First Affiliated Hospital of Dalian Medical 
      University, Dalian, Liaoning 116011, P.R. China.
FAU - Jin, Mingyu
AU  - Jin M
AD  - Department of Cardiology, The First Affiliated Hospital of Dalian Medical 
      University, Dalian, Liaoning 116011, P.R. China.
FAU - Wang, Shujing
AU  - Wang S
AD  - Department of Biochemistry and Molecular Biology, Dalian Medical University, 
      Dalian, Liaoning 116044, P.R. China.
FAU - Zhang, Jianing
AU  - Zhang J
AD  - College of Life Sciences and Pharmacy, Dalian University of Technology, Dalian, 
      Liaoning 116027, P.R. China.
FAU - Song, Xiantao
AU  - Song X
AD  - Department of Cardiology, Capital Medical University Affiliated Beijing Anzhen 
      Hospital, Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing 
      100029, P.R. China.
FAU - Huang, Rongchong
AU  - Huang R
AD  - Department of Cardiology, The First Affiliated Hospital of Dalian Medical 
      University, Dalian, Liaoning 116011, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20170823
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Antigens, CD)
RN  - 0 (Apolipoproteins E)
RN  - 0 (Cytokines)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Antigens, CD/genetics/immunology
MH  - Aorta/immunology/pathology
MH  - Apolipoproteins E/*deficiency/genetics
MH  - Atherosclerosis/genetics/*immunology/pathology
MH  - Cytokines/genetics/immunology
MH  - Dendritic Cells/cytology/immunology/*transplantation
MH  - Female
MH  - Gene Expression Regulation
MH  - Injections, Subcutaneous
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Plaque, Atherosclerotic/genetics/*immunology/pathology
MH  - Signal Transduction
MH  - Toll-Like Receptor 4/agonists/genetics/*immunology
PMC - PMC5865807
EDAT- 2017/08/30 06:00
MHDA- 2018/06/08 06:00
PMCR- 2017/08/23
CRDT- 2017/08/30 06:00
PHST- 2017/03/18 00:00 [received]
PHST- 2017/07/28 00:00 [accepted]
PHST- 2017/08/30 06:00 [pubmed]
PHST- 2018/06/08 06:00 [medline]
PHST- 2017/08/30 06:00 [entrez]
PHST- 2017/08/23 00:00 [pmc-release]
AID - mmr-16-05-6041 [pii]
AID - 10.3892/mmr.2017.7339 [doi]
PST - ppublish
SO  - Mol Med Rep. 2017 Nov;16(5):6041-6049. doi: 10.3892/mmr.2017.7339. Epub 2017 Aug 
      23.