Inhibition of p38α MAPK rescues cardiomyopathy induced by overexpressed β₂-adrenergic receptor, but not β₁-adrenergic receptor
J. Clin. Invest. Pallavi S. Peter, et al. 117:1335 doi:10.1172/JCI29576 [Go to this article.]

Figure 4
p38 and MAPKAPK2. (A) Total p38 MAPK levels were significantly higher due to transgene expression in both old bigenic β₁-AR Tg × DNp38α MAPK and old β₂-AR Tg × DNp38α MAPK mice compared with old β₁-AR Tg and old β₂-AR Tg mice, respectively, as well as with old WT mice. (B) Levels of p-p38 MAPK increased significantly in old β₁-AR Tg and old β₂-AR Tg mice compared with age-matched WT mice and were not increased in bigenic mice. (C) Total MAPKAPK2 levels were significantly higher in old bigenic β₁-AR Tg × DNp38α MAPK, old bigenic β₂-AR Tg × DNp38α MAPK mice, and DNp38α mice compared with age-matched WT mice. Both bigenic groups had levels significantly higher than those of their corresponding Tg groups. (D) Levels of p-MAPKAPK2 increased significantly in old β₁-AR Tg and old β₂-AR Tg mice compared with age-matched WT mice and were not increased in old bigenic mice. DNp38α mice were used as controls. n = 4 mice per group, with the exception of β₁-AR Tg mice in C and D (n = 5). *P < 0.05 versus WT; ^†P < 0.05 versus corresponding Tg.