The R21C Mutation in Cardiac Troponin I Imposes Differences in Contractile Force Generation between the Left and Right Ventricles of Knock-In Mice

Figure 2

The effect of the HCM-R21C mutation in cTnI on steady-state force development in LV versus RV papillary muscle strips in genetically altered mice. (a) Maximal tension per cross-section of muscle strip. Note that the R21C mutation in cTnI imposes differences in maximal steady-state force in the LV but not in RV. Sixteen to thirty independent measurements on skinned cardiac muscle strips from the left and right ventricles of three WT hearts and four homozygous R21C^+/+ knock-in hearts have been performed. ~8-month-old mice were used yielding, respectively, and muscle strips from the LV and RV of WT mice and muscle strips from LV and RV of R21C^+/+ mice. Error bars are SEM. (b) Representative force traces in the LV and RV papillary muscle fibers of R21C^+/+ mice.

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