Dihydrotestosterone suppresses female foam cells formation via inhibiting LOX-1 expression

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 355-388-Sex Hormone Receptor Action & Reaction
Basic/Translational
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-384
Yang Qiu*1, Toshihiko Yanase2, Tomoko Tanaka3, Bingqing Hu4 and Ling Li4
1Shegjing Hospital of China Medical University, Shenyang, China, 2Fukuoka University, Schl of Med., Fukuoka, Japan, 3School of Medicine, Fukuoka University, Fukuoka, Japan, 4Shengjing Hospital of China Medical University, shenyang, China
The mechanisms involved in the antiatherosclerotic effects of androgens are unclear. Men have a greater incidence of cardiovascular disease (CVD) than pre-menopausal women of similar age, but the incidence in women becomes closer to that of men after menopause. These suggest sex hormone be involved  in atherosclerosis. Although activated lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) transforms macrophages into foam cells to form the atherosclerotic plaque, and plays critical roles in atherosclerosis, the effects of androgen on female foam cells formation has not been examined, now 5a-dihydrotestosterone (DHT) suppresses male foam cells formation has been reported. Therefore, to investigate the effects of DHT on LOX-1 expression and foam cells formation in cultured female murine macrophage cell line J774.1, firstly, androgen receptor (AR) expression in J774.1 was detected by PT-PCR. Secondly, OxLDL-induced expressions of LOX-1 was significantly suppressed by 10–8M DHT by real-time PCR and Western blotting. Thirdly, 10-8M DHT inhibited formation of  macrophage-derived foam cells by oil red O staining. In conclusion, DHT inhibited female foam cell formation of macrophage via the suppression of LOX-1 expression.

Nothing to Disclose: YQ, TY, TT, BH, LL

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm