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Androgen receptor-dependent and independent atheroprotection by testosterone in male mice.

Artikel i vetenskaplig tidskrift
Författare Johan Bourghardt Fagman
Anna S K Wilhelmson
Camilla Alexanderson
Karel De Gendt
Guido Verhoeven
Alexandra Krettek
Claes Ohlsson
Åsa Tivesten
Publicerad i Endocrinology
Volym 151
Nummer/häfte 11
Sidor 5428-37
ISSN 1945-7170
Publiceringsår 2010
Publicerad vid Wallenberglaboratoriet
Centre for Bone and Arthritis Research
Institutionen för medicin, avdelningen för invärtesmedicin
Sidor 5428-37
Språk en
Länkar dx.doi.org/10.1210/en.2010-0663
Ämnesord Animals, Aorta, drug effects, metabolism, Aortic Diseases, genetics, metabolism, prevention & control, Apolipoproteins E, genetics, metabolism, Atherosclerosis, genetics, metabolism, prevention & control, Blood Pressure, physiology, Cytokines, blood, Lipids, blood, Male, Mice, Mice, Knockout, Orchiectomy, Receptors, Androgen, genetics, metabolism, Reverse Transcriptase Polymerase Chain Reaction, Statistics, Nonparametric, Testosterone, metabolism, pharmacology
Ämneskategorier Endokrinologi

Sammanfattning

The atheroprotective effect of testosterone is thought to require aromatization of testosterone to estradiol, but no study has adequately addressed the role of the androgen receptor (AR), the major pathway for the physiological effects of testosterone. We used AR knockout (ARKO) mice on apolipoprotein E-deficient background to study the role of the AR in testosterone atheroprotection in male mice. Because ARKO mice are testosterone deficient, we sham operated or orchiectomized (Orx) the mice before puberty, and Orx mice were supplemented with placebo or a physiological testosterone dose. From 8 to 16 wk of age, the mice consumed a high-fat diet. In the aortic root, ARKO mice showed increased atherosclerotic lesion area (+80%, P < 0.05). Compared with placebo, testosterone reduced lesion area both in Orx wild-type (WT) mice (by 50%, P < 0.001) and ARKO mice (by 24%, P < 0.05). However, lesion area was larger in testosterone-supplemented ARKO compared with testosterone-supplemented WT mice (+57%, P < 0.05). In WT mice, testosterone reduced the presence of a necrotic core in the plaque (80% among placebo-treated vs. 12% among testosterone-treated mice; P < 0.05), whereas there was no significant effect in ARKO mice (P = 0.20). In conclusion, ARKO mice on apolipoprotein E-deficient background display accelerated atherosclerosis. Testosterone treatment reduced atherosclerosis in both WT and ARKO mice. However, the effect on lesion area and complexity was more pronounced in WT than in ARKO mice, and lesion area was larger in ARKO mice even after testosterone supplementation. These results are consistent with an AR-dependent as well as an AR-independent component of testosterone atheroprotection in male mice.

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