PMID- 30927265
OWN - NLM
STAT- MEDLINE
DCOM- 20200526
LR  - 20200526
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 234
IP  - 10
DP  - 2019 Aug
TI  - Iron-load exacerbates the severity of atherosclerosis via inducing inflammation 
      and enhancing the glycolysis in macrophages.
PG  - 18792-18800
LID - 10.1002/jcp.28518 [doi]
AB  - Atherosclerosis is still the major cause of morbidity and mortality all over the 
      world. Recently, it has been reported increased levels of tissue iron increase 
      the risk of atherosclerosis. However, the detailed mechanism of iron-induced 
      atherosclerosis progression is barely known. Here, we used apoE-deficient mice 
      models to investigate the effects of low iron diet (<0 mg iron carbonyl/kg), high 
      iron diet (25,000 mg iron carbonyl/kg) on atherosclerosis in vivo. As exhibited, 
      we observed that CD68 was significant enriched by high iron diet in 
      apoE-deficient mice. In addition, transforming growth factor beta, tumor necrosis 
      factor alpha, interleukin 6 (IL-6), IL-23, IL-10, and IL-1beta levels were also greatly 
      induced by high iron diet. Then, we found that the iron load promoted the 
      inflammation response in macrophages. Moreover, macrophage polarization is a 
      process by which macrophage can express various functional programs in activating 
      macrophages. Here, we observed that iron-load macrophages were polarized toward a 
      proinflammatory macrophage phenotype. The polarization of M1 macrophage was 
      promoted by ferric ammonium citrate (FAC) in bone marrow derived macrophages 
      (BMDMs). Furthermore, ECAR and cellular OCR in BMDM with or without FAC was 
      examined. As shown, BMDM indicated with 50 muM FAC showed a significant increase 
      in basic state and maximal ECAR in contrast to the control group. However, there 
      was no significant difference in OCR. This indicated that the glycolysis was 
      involved in the polarization of M1 macrophage triggered by iron-load. In 
      conclusion, we indicated that the iron load exacerbates the progression of 
      atherosclerosis via inducing inflammation and enhancing glycolysis in 
      macrophages.
CI  - (c) 2019 Wiley Periodicals, Inc.
FAU - Hu, Xiaorong
AU  - Hu X
AUID- ORCID: 0000-0002-9378-3715
AD  - Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 
      People's Republic of China.
FAU - Cai, Xinyong
AU  - Cai X
AD  - Department of Cardiology, Jiangxi Provincial People's Hospital Affiliated to 
      Nanchang University, Nanchang, Jiangxi, People's Republic of China.
FAU - Ma, Ruisong
AU  - Ma R
AD  - Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 
      People's Republic of China.
FAU - Fu, Wenwen
AU  - Fu W
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei, People's Republic of China.
FAU - Zhang, Changjiang
AU  - Zhang C
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei, People's Republic of China.
FAU - Du, Xianjin
AU  - Du X
AUID- ORCID: 0000-0002-2558-7982
AD  - Department of Emergency, Renmin Hospital of Wuhan University, Wuhan, Hubei, 
      People's Republic of China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190329
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Ferric Compounds)
RN  - E1UOL152H7 (Iron)
RN  - LUX2X1H1IC (ammonium ferric sulfate)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/complications/*pathology
MH  - Cell Polarity
MH  - Female
MH  - Ferric Compounds/adverse effects
MH  - *Glycolysis
MH  - Inflammation/complications/*pathology
MH  - Iron/*adverse effects
MH  - Macrophages/*metabolism/pathology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Phenotype
MH  - *Severity of Illness Index
OTO - NOTNLM
OT  - atherosclerosis
OT  - glycolysis
OT  - inflammation
OT  - iron
EDAT- 2019/03/31 06:00
MHDA- 2020/05/27 06:00
CRDT- 2019/03/31 06:00
PHST- 2018/12/20 00:00 [received]
PHST- 2019/02/22 00:00 [revised]
PHST- 2019/03/05 00:00 [accepted]
PHST- 2019/03/31 06:00 [pubmed]
PHST- 2020/05/27 06:00 [medline]
PHST- 2019/03/31 06:00 [entrez]
AID - 10.1002/jcp.28518 [doi]
PST - ppublish
SO  - J Cell Physiol. 2019 Aug;234(10):18792-18800. doi: 10.1002/jcp.28518. Epub 2019 
      Mar 29.