PMID- 34581005
OWN - NLM
STAT- MEDLINE
DCOM- 20220316
LR  - 20220316
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Print)
IS  - 1582-1838 (Linking)
VI  - 25
IP  - 21
DP  - 2021 Nov
TI  - Interleukin-7 aggravates myocardial ischaemia/reperfusion injury by regulating 
      macrophage infiltration and polarization.
PG  - 9939-9952
LID - 10.1111/jcmm.16335 [doi]
AB  - Interleukin (IL)-7 is known to enhance the macrophages cytotoxic activity and 
      that macrophages play a pivotal role in the development and progression of 
      myocardial ischaemia/reperfusion (I/R) injury. However, the effects of IL-7 on 
      macrophages infiltration and polarization in myocardial I/R injury are currently 
      unclear. This study aimed to evaluate the effects of the IL-7 expression on 
      myocardial I/R injury and their relationship with macrophages. The data showed 
      that IL-7 expression in mouse heart tissue increases following I/R injury and 
      that IL-7 knockout or anti-IL-7 antibody treatment significantly improve I/R 
      injury, including reduction in myocardial infarction area, a serum troponin T 
      level decreases and an improvement in cardiac function. On the other hand, 
      recombinant IL-7 (rIL-7) supplementation induces opposite effects and the 
      anti-IL-7 antibody significantly reduces the cardiomyocyte apoptosis and 
      macrophage infiltration. rIL-7 cannot directly cause apoptosis, but it can induce 
      cardiomyocyte apoptosis through macrophages, in addition to increase the 
      macrophages migration in vitro. Anti-IL-7 antibody affects the cytokine 
      production in T helper (Th) 1 and Th2 cells and also promotes the macrophages 
      differentiation to M2 macrophages. However, anti-IL-7 antibody does not reduce 
      the M1 macrophage number, and it only increases the ratio of M2/M1 macrophages in 
      mice heart tissues after I/R injury. Taking together, these data reveal that IL-7 
      plays an intensifying role in myocardial I/R injury by promoting cardiomyocyte 
      apoptosis through the regulation of macrophage infiltration and polarization.
CI  - (c) 2021 The Authors. Journal of Cellular and Molecular Medicine published by 
      Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
FAU - Yan, Mengwen
AU  - Yan M
AD  - Department of Cardiology, China-Japan Friendship Hospital, Beijing, China.
FAU - Yang, Yaliu
AU  - Yang Y
AD  - Department of Cardiology, China-Japan Friendship Hospital, Beijing, China.
FAU - Zhou, Ying
AU  - Zhou Y
AD  - Department of Cardiology, China-Japan Friendship Hospital, Beijing, China.
FAU - Yu, Changan
AU  - Yu C
AD  - Central Laboratory of Cardiovascular Disease, China-Japan Friendship Hospital, 
      Beijing, China.
FAU - Li, Rui
AU  - Li R
AD  - Department of Health Care, China-Japan Freindship Hospital, Ministry of Health, 
      Beijing, China.
FAU - Gong, Wei
AU  - Gong W
AUID- ORCID: 0000-0002-3298-7001
AD  - Emergency and Critical Care Center, Beijing Anzhen Hospital Capital Medical 
      University, Beijing, China.
AD  - Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing, China.
FAU - Zheng, Jingang
AU  - Zheng J
AD  - Department of Cardiology, China-Japan Friendship Hospital, Beijing, China.
AD  - Department of Cardiology, China-Japan Friendship School of Clinical Medicine, 
      Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 
      China.
AD  - Department of Cardiology, Peking University China-Japan Friendship School of 
      Clinical Medicine, Beijing, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210928
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (Biomarkers)
RN  - 0 (Interleukin-7)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Biomarkers
MH  - Disease Models, Animal
MH  - Disease Susceptibility
MH  - Gene Expression
MH  - Heart Function Tests
MH  - Hemodynamics
MH  - Immunophenotyping
MH  - Interleukin-7/genetics/*metabolism
MH  - Macrophage Activation/*immunology
MH  - Macrophages/*immunology/*metabolism/pathology
MH  - Mice
MH  - Mice, Knockout
MH  - Myocardial Reperfusion Injury/diagnosis/*etiology/*metabolism
MH  - Myocytes, Cardiac/metabolism
PMC - PMC8572772
OTO - NOTNLM
OT  - interleukin-7
OT  - ischaemia/reperfusion injury
OT  - macrophage
OT  - myocardial
COIS- None.
EDAT- 2021/09/29 06:00
MHDA- 2022/03/17 06:00
PMCR- 2021/11/01
CRDT- 2021/09/28 07:01
PHST- 2020/12/23 00:00 [revised]
PHST- 2020/09/08 00:00 [received]
PHST- 2020/12/28 00:00 [accepted]
PHST- 2021/09/29 06:00 [pubmed]
PHST- 2022/03/17 06:00 [medline]
PHST- 2021/09/28 07:01 [entrez]
PHST- 2021/11/01 00:00 [pmc-release]
AID - JCMM16335 [pii]
AID - 10.1111/jcmm.16335 [doi]
PST - ppublish
SO  - J Cell Mol Med. 2021 Nov;25(21):9939-9952. doi: 10.1111/jcmm.16335. Epub 2021 Sep 
      28.