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Myocardial IL‐6R expression and IL‐6 signaling following exercise
Author(s) -
McGinnis Graham Ripley,
Barberio Matthew,
Ballmann Christopher,
Peters Bridget,
Quindry John,
Amin Rajesh
Publication year - 2013
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.27.1_supplement.lb775
Subject(s) - stat3 , medicine , endocrinology , stat protein , skeletal muscle , interleukin 6 , treadmill , chemistry , phosphorylation , inflammation , biochemistry
Interleukin‐6 (IL‐6) is produced in and released from skeletal muscle during contraction. IL‐6 activity is regulated by a signaling complex with the IL‐6 receptor (IL‐6R). Basal expression of IL‐6R is minimal, but increases with exercise in skeletal muscle. The purpose of this study was to determine if exercise increases myocardial IL‐6R expression, and increases phosphorylation of signal transducer and activator of transcription (STAT3) in the heart. Wild type (WT, n=18) and IL‐6 knock‐out (KO, n=12) mice were grouped as sedentary or exercised. Mice were habituated to treadmill exercise for 4 days increasing from 10–40 min bouts. After 1 d rest, mice performed 3 d exercise for 60 min at 18 m/min. Sedentary animals had equal treadmill time at 0 m/min. Mice were sacrificed pre‐, 0, 30 and 60 min post exercise. Heart, gastroc and plasma were collected, snap frozen and stored at −80°C. Samples were normalized for protein concentration and probed for IL‐6R and P‐STAT3. IL‐6R increased post‐exercise in gastroc (~140%), heart (~250%) and plasma (~300%) in WT only. P‐STAT3 in gastroc increased (~18%) in both WT and KO. Minor increase in P‐STAT3 in heart (~10%) was only in WT. Further study is needed to confirm present findings. It appears exercise causes IL‐6/IL‐6R mediated STAT3 activation in the heart. Findings suggest that alternative cytokines may compensate for lack of IL‐6 in the KO mice. [JCQ Level 3 IGP 2011]