Research Paper Volume 2, Issue 8 pp 504—513

Muscle-specific inositide phosphatase (MIP/MTMR14) is reduced with age and its loss accelerates skeletal muscle aging process by altering calcium homeostasis

class="figure-viewer-img"

Figure 2. Evidence for muscle atrophy, decreased contractile force, and reduced power in skeletal muscles suggested similarity from old WT and MIPKO mice. In all figures, the black bars are mature, wild type mice, the red bars are old, wild type mice, the green bars are mature MIPKO mice, and the blue bars are old, MIPKO mice. (A) Typical Toluidine blue-stained cross sections of EDL muscles from young Wt, old Wt, and mature MIPKO mice. The cross-sectional areas of old Wt and MIPKO cells are significantly reduced compared with those of the young Wt. (B) Maximal contractile force in EDL muscle for each genotype. Atrophy (decrease in muscle cross-sectional area) can explain ~ 1/2 of the drop in total force (note the dotted horizontal line), but does not account for the complete decrease in contractile force. (C) Data from B, except that force is normalized per cross-sectional area (N/cm2). This figure illustrates the atrophy-independent component of contractile dysfunction. (D) Maximal power in EDL muscle from all four animal models. (E) Data from panel D was normalized per cross sectional area of muscles. It shows that a significant drop in power is atrophy-independent. Data is the average ± SE of 24 EDL muscles from 12 mice for each genotype. * indicates a significant difference (p < 0.01) between the control muscles and a particular genotype. ** indicates a significant difference (p < 0.01) between the old MIPKO mice and the old Wt and mature MIPKO mice.