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

Figure 4

Passive tension per cross-section of muscle strip in LV and RV of R21C^+/+ mice compared with LV and RV of WT mice. After skinning the strips were washed in the relaxing solution and their length was adjusted to remove the slack to sarcomere length (SL) = ~2.1 µm. This point was set as zero for both the passive force and starting length of the muscle strip. Then, the strips were stretched by 10% of its length ×4 consecutive times, and the passive force per cross-section of muscle (in kN/m²) was determined. Note that the R21C mutation exerted its effect on passive tension in the LV compared to LV-WT ( as established by repeated measures ANOVA). The values of passive tension (in kN/m²) for 10%, 20%, 30%, and 40% stretch were ; ; ; and for LV-WT and ; ; ; and for LV-R21C^+/+. No statistical differences in the resistance to stretch were observed between the LV versus RV of WT mice. Interestingly, the passive tension for 10% stretch (in kN/m²) was (LV-WT); (RV-WT); (LV-R21C^+/+); and (RV-R21C^+/+). The difference between LV-mutant and LV-WT was statistically significant () indicating mutation-induced partial loss of Ca²⁺ regulation at low Ca²⁺. Data are average of = 9-10 experiments performed on skinned muscle strips from 9-month-old male mice. Error bars are SEM.