M2b macrophages reduce early reperfusion injury after myocardial ischemia in mice: A predominant role of inhibiting apoptosis via A20. (15th October 2017)

• Record Type: Journal Article
• Authors: Yue, Yuan; Yang, Xiao; Feng, Kangni; Wang, Lexun; Hou, Jian; Mei, Bo; Qin, Han; Liang, Mengya; Chen, Guangxian; Wu, Zhongkai
• Is Part Of: International journal of cardiology. Volume 245(2017)
• Page Start: 228
• Page End: 235
• Publication Date: 2017-10-15
• Subjects: Ischemia/reperfusion injury -- Myocardial ischemia -- Macrophage -- Apoptosis -- A20; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2017.07.085
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: 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 1 × 10 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-κB (NF-κB) signaling activation in the MT group after 2 h 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-κB signaling-mediated apoptosis.