Overexpression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by inhibiting PI3K/Akt signaling in mice

• DOI: 10.1097/hjh.0b013e3283505101
• Publication Date: 2012-02-16T13:54:49Z
• Authors: Shigeki Sagara; Tomohiro Osanai; Taihei Itoh; Kei Izumiyama; Shuji Shibutani; Kenji Hanada; Hiroaki Yokoyama; Yuko Yamamoto; Takashi Yokota; Hirofumi Tomita; Koji Magota; Ken Okumura
• Keywords: Ventricular hypertrophy

Background: Regular exercise improves systolic cardiac dysfunction through Akt cascade-mediated physiological hypertrophy in congestive heart failure. Tissue acidosis impairs cascade, and coupling factor 6 induces tissue via activation of ecto-F1Fo complex. We tested the hypothesis that attenuates induced by its benefit mice. Methods results: Adult wild-type mice (n = 20) 6-overexpressing transgenic were divided into two groups with or without 4-week consisting 90-min swimming twice daily. Left ventricular posterior wall interventricular septum thicknesses increased 0.12 ± 0.1 0.16 mm, respectively, after (both P < 0.01), but unchanged Fractional shortening was from 37 1 to 41 1% (P 0.05), whereas it transgenic. The insulin-like growth (IGF-1) receptor protein phosphorylated form both 1.83 0.23 0.09 times, Downstream phosphoinsulin substrate 1, phosphoinositide 3-kinase, phospho-Akt 2.22 0.22, 1.78 0.31, 2.24 0.49 (all Restoration IGF-1 injection recovered left function Conclusion: Overexpression exercise-induced downregulating signaling, thereby cancelling for Reduction level seems be useful drawing exercising effects on function.