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Angiomotin isoforms are differentially affected by exercise training in skeletal muscles from lean and obese rats
Author(s) -
BIROT Olivier,
FORN Paul,
ROUDIER Emilie
Publication year - 2009
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.23.1_supplement.625.2
Subject(s) - angiogenesis , gene isoform , skeletal muscle , endocrinology , pathological , medicine , phenotype , context (archaeology) , soleus muscle , biology , biochemistry , gene , paleontology
Angiomotin (Amot) was recently identified on the surface of endothelial cells, regulating their migration and thus angiogenesis. p80 Amot isoform is mostly expressed in the dynamic phase of angiogenesis when activated endothelial cells migrate, whereas p130 is more characteristic of stabilized vessels. Such observations were mainly obtained from studies on pathological angiogenesis and the physiological regulation of Amot in healthy tissues remains largely unknown. Objectives To study 1) whether Amot was physiologically expressed in skeletal muscle, 2) how physical activity, a pro‐angiogenic physiological stimulus in skeletal muscle, could regulate Amot expression, 3) if such regulation was altered in the context of obesity. Methods p80 and p130 expressions were measured in soleus and plantaris from sedentary and trained, lean or obese rats. Results Exercise training shifted Amot isoforms expression pattern toward an "angiogenic phenotype". However, such regulation was different between lean and obese rats. In lean animals, exercise training increased p80 expression, whereas in obese rats it reduced p130. Conclusion p80/p130 ratio could reflect the tissue angiogenic potential. Exercise shifted this Amot isoforms ratio toward an angiogenic phenotype by different mechanisms between lean and obese rats. This work was supported by the Natural Sciences and Engineering Research Council of Canada.