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. 2013 Dec 19;2(6):e000439. doi: 10.1161/JAHA.113.000439

Figure 9.

Figure 9.

A through F, Cardiomyocyte contractile properties of WT and MIF−/− mice treated with rmMIF reconstitution or rapamycin in the presence or absence of the lysosomal inhibitor bafilomycin A1 (BafA1, 3 μmol/kg per day, i.p.) for 7 days immediately following initiation of rmMIF or rapamycin treatment. A, Resting cell length; B, peak shortening (PS, normalized to resting cell length); C, +dL/dt; D, −dL/dt; E, TPS; F, TR90. Mean±SEM, n=100 to 130 cells from 5 mice per group, *P<0.05 vs WT group, #P<0.05 vs WT DOX group, †P<0.05 vs MIFko DOX group. G through K, Effect of rmMIF reconstitution on myocardial autophagy flux in MIF−/− mice treated with or without DOX. G, Representative gel blots depicting protein levels of LC3BI/II, p62 and GAPDH (loading control) using specific antibodies; H, LC3B I expression; I, LC3B II expression; J, LC3B II‐to‐LC3B I ratio; K, p62 expression. Mean±SEM, n=5 to 6 mice per group, *P<0.05 vs WT group, #P<0.05 vs WT DOX group. BafA1 indiactes bafilomycin A1; +dL/dt, maximal velocity of shortening; −dL/dt, maximal velocity of relengthening; DOX, doxorubicin; i.p., intraperitoneal; ko, knockout; MIF, macrophage migration inhibitory factor; Rapa, rapamycin; rmMIF, recombinant mouse macrophage migration inhibitory factor; TPS, time‐to‐PS; TR90, time‐to‐90% relengthening; WT, wild type.