- MerTK Cleavage on Resident Cardiac Macrophages Compromises Repair After Myocardial Ischemia Reperfusion Injury.
MerTK Cleavage on Resident Cardiac Macrophages Compromises Repair After Myocardial Ischemia Reperfusion Injury.
Circulation research (2017-08-31)
Matthew DeBerge, Xin Yi Yeap, Shirley Dehn, Shuang Zhang, Lubov Grigoryeva, Sol Misener, Daniel Procissi, Xin Zhou, Daniel C Lee, William A Muller, Xunrong Luo, Carla Rothlin, Ira Tabas, Edward B Thorp
PMID28851810
摘要
Clinical benefits of reperfusion after myocardial infarction are offset by maladaptive innate immune cell function, and therapeutic interventions are lacking. We sought to test the significance of phagocytic clearance by resident and recruited phagocytes after myocardial ischemia reperfusion. In humans, we discovered that clinical reperfusion after myocardial infarction led to significant elevation of the soluble form of MerTK (myeloid-epithelial-reproductive tyrosine kinase; ie, soluble MER), a critical biomarker of compromised phagocytosis by innate macrophages. In reperfused mice, macrophage Our data implicate monocyte-induced MerTK cleavage on proreparative MHCII
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