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.