PMID- 28764858
OWN - NLM
STAT- MEDLINE
DCOM- 20180514
LR  - 20180514
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 245
DP  - 2017 Oct 15
TI  - M2b macrophages reduce early reperfusion injury after myocardial ischemia in 
      mice: A predominant role of inhibiting apoptosis via A20.
PG  - 228-235
LID - S0167-5273(17)31265-2 [pii]
LID - 10.1016/j.ijcard.2017.07.085 [doi]
AB  - BACKGROUND: Monocytes or macrophages have been assessed as potential therapeutics 
      to ameliorate myocardial ischemic diseases, but the results have been 
      controversial. As regulatory macrophages, M2b macrophages could have enhanced 
      protective effects. We tested the hypothesis that transplantation of M2b 
      macrophages could ameliorate myocardial ischemia/reperfusion (I/R) injury. The 
      potential mechanisms involved in it were investigated. METHODS: M2b macrophages 
      were polarized by lipopolysaccharide (LPS) and the immune complex (IC) from bone 
      marrow-derived macrophages (BMDMs) of C57BL/6 mice. They were identified based on 
      surface marker expression and cytokine production. Myocardial I/R injury models 
      were established with the same strain of mice. Once the ischemic area was 
      identified, either 1x10(5) M2b macrophages (MT group) or the same volume of 
      normal saline (CK group) was injected into the ischemic zone. Mice in the sham 
      operation (SO) group underwent the operation without ligation of the coronary 
      artery. RESULTS: We found a significant decrease in serum cardiac troponin I 
      (cTnI) level, the infarct area, apoptosis index, and nuclear factor-kappaB (NF-kappaB) 
      signaling activation in the MT group after 2h of reperfusion; the changes were 
      induced by I/R. In addition, the injury resulted in significantly up-regulated 
      expression of A20 and continued to be improved by the transplanted M2b 
      macrophages. CONCLUSIONS: The administration of M2b macrophages significantly 
      attenuated myocardial I/R injury. A20 may be part of the protective mechanism 
      through limiting NF-kappaB signaling-mediated apoptosis.
CI  - Copyright (c) 2017 The Authors. Published by Elsevier B.V. All rights reserved.
FAU - Yue, Yuan
AU  - Yue Y
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Yang, Xiao
AU  - Yang X
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China; Department of 
      Laboratory Medicine, Guangzhou First People's Hospital, Affiliated Hospital of 
      Guangzhou Medical University, China.
FAU - Feng, Kangni
AU  - Feng K
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Wang, Lexun
AU  - Wang L
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Hou, Jian
AU  - Hou J
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Mei, Bo
AU  - Mei B
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Qin, Han
AU  - Qin H
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Liang, Mengya
AU  - Liang M
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Chen, Guangxian
AU  - Chen G
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China.
FAU - Wu, Zhongkai
AU  - Wu Z
AD  - The First Affiliated Hospital of Sun Yat-Sen University, China. Electronic 
      address: wuzhk@mail.sysu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20170726
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
RN  - EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
RN  - EC 3.4.22.- (Tnfaip3 protein, mouse)
SB  - IM
EIN - Int J Cardiol. 2019 Mar 1;278:311. PMID: 30503241
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Cells, Cultured
MH  - Macrophages/*metabolism/*transplantation
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myocardial Ischemia/*metabolism/therapy
MH  - Myocardial Reperfusion Injury/*metabolism/therapy
MH  - Tumor Necrosis Factor alpha-Induced Protein 3/*biosynthesis
OTO - NOTNLM
OT  - A20
OT  - Apoptosis
OT  - Ischemia/reperfusion injury
OT  - Macrophage
OT  - Myocardial ischemia
EDAT- 2017/08/03 06:00
MHDA- 2018/05/15 06:00
CRDT- 2017/08/03 06:00
PHST- 2017/03/01 00:00 [received]
PHST- 2017/07/01 00:00 [revised]
PHST- 2017/07/21 00:00 [accepted]
PHST- 2017/08/03 06:00 [pubmed]
PHST- 2018/05/15 06:00 [medline]
PHST- 2017/08/03 06:00 [entrez]
AID - S0167-5273(17)31265-2 [pii]
AID - 10.1016/j.ijcard.2017.07.085 [doi]
PST - ppublish
SO  - Int J Cardiol. 2017 Oct 15;245:228-235. doi: 10.1016/j.ijcard.2017.07.085. Epub 
      2017 Jul 26.