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Dihydrotestosterone (DHT) increases cyclooxygenase‐2 (COX‐2) in human coronary artery smooth muscle cells following IL‐1β‐induced inflammation
Author(s) -
Osterlund Kristen,
Gutierrez Anthony,
Gonzales Rayna J
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.775.17
Subject(s) - dihydrotestosterone , medicine , inflammation , endocrinology , agonist , androgen receptor , androgen , lipopolysaccharide , pathophysiology , cytokine , vascular smooth muscle , stimulation , receptor , smooth muscle , hormone , prostate cancer , cancer
Effects of androgens on normal physiological and pathophysiological vascular function remain unclear. Both protective and non‐protective effects of androgens on the cardiovascular system have been documented. Our previous studies show that chronic androgen treatment augments vascular tone under normal physiological conditions and exacerbates endotoxin‐induced inflammation in cerebral arteries isolated from rodents. Here we investigated whether dihydrotestosterone (DHT; 100nM), the more potent androgen receptor agonist, modulates COX‐2 in primary human coronary vascular smooth muscle cells following stimulation with either IL‐1β (5ng/ml) or lipopolysaccharide (LPS 100 ug/ml). A time course for cytokine‐ or endotoxin‐induced COX‐2 levels assessed via Western blot showed that COX‐2 levels were greatest at 6 and 9 hours post cytokine or endotoxin exposure. Similar to IL‐1β or LPS, DHT treatment increased COX‐2 protein compared to vehicle. Interestingly, LPS induced increases in COX‐2 levels were blunted when administered concomitantly with DHT. In conclusion, androgens may have a differential impact on inflammation during pathophysiological compared to normal physiological conditions. Support: AHA SDG RG