MerTK Cleavage on Resident Cardiac Macrophages Compromises Repair After Myocardial Ischemia Reperfusion Injury.

ABSTRACT:

Rationale

Clinical benefits of reperfusion after myocardial infarction are offset by maladaptive innate immune cell function, and therapeutic interventions are lacking.

Objective

We sought to test the significance of phagocytic clearance by resident and recruited phagocytes after myocardial ischemia reperfusion.

Methods and results

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 Mertk deficiency led to decreased cardiac wound debridement, increased infarct size, and depressed cardiac function, newly implic

SUBMITTER: DeBerge M 

PROVIDER: S-EPMC5623080 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature