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. 2018 May 28;9:558. doi: 10.3389/fphys.2018.00558

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Copyright © 2018 Schiattarella, Boccella, Paolillo, Cattaneo, Trimarco, Franzone, D’Apice, Giugliano, Rinaldi, Borzacchiello, Gentile, Lombardi, Feliciello, Esposito and Perrino.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Siah2 deficiency prevents AKAP121 degradation after TAC. (A) Representative immunoblot (left) and densitometric analysis (right) of AKAP121 protein levels in wt and Siah2^-/- hearts 1 week after sham or TAC procedure. GAPDH was used as control of loading sample (^∗p < 0.05 vs. wt sham). (B) Bar graphs showing cumulative data of LVW/ BW 1 week after sham or TAC procedures in wt and Siah2^-/- mice (^∗p < 0.05 vs. sham; n = 6 hearts/group). Cumulative data of % fractional shortening (C), left ventricular end-systolic diameter (LVESd; D), and left ventricular end-diastolic diameter (LVEDd; E) in wt and Siah2^-/- mice 1 week after sham or TAC procedure (^∗p < 0.05 vs. sham; n = 6 hearts/group).