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- W2488147030 abstract "Increasing titin length in the heart through functional deletion of the RNA recognition motif (RRM) of RBM20 protein leads to a reduction of left ventricular (LV) chamber stiffness in sedentary mice. We tested the therapeutic effect of upregulating compliant titins by creating diastolic dysfunction in a mouse model with inducible RBM20 inhibition (MerCreMer;cRbm20ΔRRM). Under transcriptional control of an MHC6 promoter, RBM20 function of MerCreMer;cRbm20ΔRRM mice was inhibited in time- and cardiac-specific manners.Adult male MerCreMer;cRbm20ΔRRM mice had undergone transaortic constriction (TAC) surgery with Deoxycorticosterone acetate (DOCA) pellet implantation. Two weeks after TAC+DOCA surgery, mice developed LV hypertrophy and diastolic dysfunction as demonstrated by echocardiography. Four weeks after surgery, pressure volume analysis revealed that LV chamber stiffness was markedly increased in TAC+DOCA mice (140% increased versus sham). However, the TAC+DOCA mice with RBM20 inhibition developed less severe LV chamber stiffness (29% increased versus sham). Passive stiffness measurements showed a reduction of cardiomyocyte stiffness in TAC+DOCA mice with RBM20 inhibition.Inhibition of the RBM20-based splicing system results in expression of compliant mutant N2BA titin which consequently lead to a reduction of cardiomyocyte stiffness and LV chamber stiffness in a mouse model with diastolic dysfunction." @default.
- W2488147030 created "2016-08-23" @default.
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- W2488147030 date "2016-02-01" @default.
- W2488147030 modified "2023-10-05" @default.
- W2488147030 title "Upregulating Compliant Titin in the Heart Attenuates Left Ventricular Stiffness in a Mouse Model with Diastolic Dysfunction" @default.
- W2488147030 doi "https://doi.org/10.1016/j.bpj.2015.11.1605" @default.
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