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Cyclooxygenase mRNA expression in human patellar tendon at rest and after exercise
Author(s) -
Carroll Chad C,
Jemiolo Bozena,
Trappe Scott W,
Døssing Simon,
Kjaer Michael,
Magnusson S Peter,
Trappe Todd A
Publication year - 2008
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.22.1_supplement.753.32
Subject(s) - cyclooxygenase , tendon , medicine , proportional hazards model , endocrinology , biopsy , patellar tendon , patellar ligament , skeletal muscle , enzyme , anatomy , biology , biochemistry
Exercise has been shown to acutely elevate several metabolic processes in tendon tissue, many of which are regulated by the cyclooxygenase (COX) enzymes. We measured the expression levels of COX‐1 (variants 1 and 2), COX‐2, and the recently discovered intron 1‐retaining COX‐1 variants (COX‐1b 1 , ‐1b 2 , ‐1b 3 ) at rest and following resistance exercise (RE). Patellar tendon biopsy samples were taken from six individuals (3M, 3F) before and 4h following a bout of RE (3 sets of 10 repetitions at ~70% of 1RM) and from a separate six individuals (3M, 3F) before and 24h following RE and analyzed using real‐time RT‐PCR. The COX‐1 variants were the most abundant COX mRNAs before exercise and remained unchanged (p>0.05) following exercise. COX‐2 was also expressed in tendon at rest and was unchanged (p>0.05) following exercise. The intron 1‐retaining COX‐1 variants were not detectable in tendon tissue before or after exercise. Compared to our previous work in quadriceps skeletal muscle, the patellar tendon expressed much higher levels of COX‐1 and COX‐2, although the overall COX mRNA expression patterns were similar in skeletal muscle and tendon (COX‐1v2 > COX‐1v1, P <0.05; COX‐1:COX‐2 ≅ 4:1). These results suggest both COX‐1 and COX‐2 are constitutively expressed at relatively high levels in human patellar tendon and are likely targets of COX inhibiting drugs at rest and following physical activity. NIH R01 AG020532 (TT)