Fig. 2.

Echocardiographic evaluation of the role of FGFR4 in FGF23-mediated LVH. FGFR4 ^flox/flox and Myhe-Cre;FGFR4^flox/flox mice were treated with tamoxifen for 7 days to create control and conditional cardiac FGFR4 knock mice. Both groups were treated with FGF23 for 5 days to induce LVH. Injection of rFGF23 (75 ng/g body weight, i.p.) for 5 days induced LVH in tamoxifen treated control mice with FGFR4 expression in the heart (A, top and B), but not in FGFR4^heart-cKO mice created by tamoxifen treatment for 7 days to delete FGFR4 in the heart (A, bottom, and D). D0 indicates analysis at baseline and D3, D5 and D7 reflect 3, 5 and 7 of Tamoxifen treatment. Tamoxifen induced cardiac FGFR4 specific deletion in a time-dependent manner, with FGFR4 progressively decreasing by 50 and 75% after tamoxifen treatment for 3 and 5 days, respectively (C). FGFR4 expression was reduce by over 90% after 7 days of tamoxifen treatment. rFGF23 induced LVH in mice treated with tamoxifen for up to 5 days when FGFR4 could still be detected, but not after 7d of tamoxifen treatment FGFR4^{flox/flox/Myh6-Cre} mice that deleted FGFR4 in the heart. Effects of deletion of cardiac FGFR4 to attenuate rFGF23-mediated LVH was further confirmed by echocardiography (E-I). FGFR4 deficiency in the heart had no effect on rFGF23 induced hypertension (J). n = 4–5/group, *p < .05 vs controls. All values are shown as mean ± S.E.