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Reductions in REDD1 expression correspond to enhanced rates of protein synthesis following eccentric contractions (1163.16)
Author(s) -
Gordon Bradley,
Steiner Jennifer,
Lang Charles,
Kimball Scot,
Jefferson Leonard
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1163.16
Subject(s) - mtorc1 , stimulation , phosphorylation , skeletal muscle , endocrinology , medicine , muscle hypertrophy , contraction (grammar) , signal transduction , pi3k/akt/mtor pathway , protein kinase b , chemistry , messenger rna , biology , microbiology and biotechnology , biochemistry , gene
Resistance exercise induces skeletal muscle hypertrophy due to enhanced rates of protein synthesis. Signaling through mTORC1 plays a vital role in integrating signals generated by resistance exercise to control skeletal muscle growth. REDD1 is a negative regulator of mTORC1 signaling whose mRNA expression is reduced in human skeletal muscle following resistance exercise. The purpose of the present study was to determine how changes in REDD1 protein expression correspond with changes in mTORC1 signaling and protein synthesis, following electrical stimulation of the sciatic nerve to induce contraction of the tibialis anterior in mice. Thirty min post stimulation, phosphorylation of p70S6K1 (T389) was increased 146% while rates of protein synthesis and REDD1 expression were unchanged compared to control. Four h post stimulation, phosphorylation of p70S6K1 (T389) was further elevated 4.5‐fold and rates of protein synthesis were increased compared to control. At this time point, REDD1 expression was reduced 40%, which was accompanied by a 71% increase in Akt (T308) phosphorylation. These data demonstrate that a reduction in REDD1 expression is not necessary for the initial, weak contraction‐induced stimulation of mTORC1 signaling. However, a subsequent fall in REDD1 expression leads to a more dramatic stimulation of mTORC1 signaling resulting in elevated rates of protein synthesis. Grant Funding Source : NIH Grants DK‐15658, GM38032