MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction

Altering inflammation can impact the recovering heart's structure and function following myocardial infarction (MI). MAP kinase‐activated protein kinase 2 (MK2) regulates the stability of several pro‐inflammatory cytokines. Hence, this study was to determine if MK2 deficiency impaired the inflammatory phase of post‐MI wound repair. Myocardial infarctions were induced by permanent ligation of the left anterior descending coronary artery in 12‐week‐old male MK2 +/+ and MK2 −/− mice. Five days post‐MI, survival was 100% in MI‐MK2 −/− ( n = 20) and 79% in MI‐MK2 +/+ mice ( n = 29; Mandel‐Cox test: p < 0.05). Systolic and diastolic LV diameters were greater in MI‐MK2 +/+ than MI‐MK2 −/− mice. Infiltration of neutrophils or monocytes did not differ significantly. Cytokine and chemokine transcripts were quantified in infarcted and non‐infarcted LV tissue using qPCR arrays. Three days post‐MI, Ifna2 was increased and Il16 was decreased in infarcted tissue from MK2 −/− hearts, compared with infarcted MK2 +/+ tissue, whereas in the non‐infarcted MK2 −/− myocardium Il27 increased and Tnfsf11 , Ccl3 , and Il1rn were decreased. Five days post‐MI, Ctf16 and Il10 increased in infarcted MK2 −/− tissue whereas in the non‐infarcted MK2 −/− myocardium Ccl9 , Nodal , and Xcl2 increased and Il15 decreased. These findings suggest MK2 deficiency is an advantage during the inflammatory phase of cardiac wound repair post‐MI.