徳島大学 教育・研究者情報データベース(EDB)

1. 池田 康将([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.薬理学]/[徳島大学.医学部.医学科.病態情報医学講座.薬理学分野]/[徳島大学.医科学教育部.医学専攻.病態情報医学講座]/[徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.薬理学])

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2. 粟飯原 賢一([徳島大学.大学院医歯薬学研究部.医学域.連携研究部門(医学域).寄附講座系(医学域).実践地域診療・医科学])

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3. 吉田 守美子([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.血液・内分泌代謝内科学])

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4. (英) Sato Takashi

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5. (英) Yagi Shusuke

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6. (英) Iwase Takashi

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7. (英) Sumitomo Yuka

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8. (英) Ise Takayuki

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9. (英) Ishikawa Kazue

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10. (英) Azuma Hiroyuki

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11. (英) Akaike Masashi

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12. (英) Kato Shigeaki

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13. (英) Matsumoto Toshio

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(英) Androgen-androgen receptor system protects against angiotensin II-induced vascular remodeling.

(英) Age-related andropause promotes cardiovascular disease in males. Although we had previously reported that the androgen-androgen receptor (AR) system plays important roles in cardiac growth and remodeling, the system's involvement in vascular remodeling remains unclear. To clarify this role, 25-wk-old male AR knockout (ARKO) mice and littermate male wild-type (WT) mice were divided into two groups with and without angiotensin II (Ang II) administration (2.0 mg/kg . d) for 14 d, respectively. No morphological differences in the coronary artery and thoracic aorta were observed between the groups without Ang II. Ang II stimulation markedly increased medial thickness and perivascular fibrosis in ARKO mice, with enhanced TGF-beta1, collagen type I, and collagen type III gene expression in the aorta. Ang II stimulation also prominently increased superoxide production, lipid peroxidation, and gene expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components in ARKO mice compared with WT mice. In addition, phosphorylation of c-Jun N-terminal kinase (JNK) and phosphorylated (Smad2/3) was remarkably enhanced in Ang II-treated ARKO mice compared with Ang II-treated WT mice. Notably, daily urinary nitric oxide (NO) metabolites excretion as a marker of NO bioavailability, aortic endothelial NO synthase expression and phosphorylation, and Akt phosphorylation were significantly reduced in ARKO mice compared with WT mice, regardless of Ang II stimulation. In conclusion, the androgen-AR system is required for the preservation of NO bioavailability through Akt-endothelial NO synthase system activation and exerts protective effects against Ang II-induced vascular remodeling by regulating oxidative stress, c-Jun N-terminal kinase (JNK) signaling, and the TGF-beta-phosphorylated Smad pathway.

1. (英) Androgens
2. (英) Angiotensin II
3. (英) Animals
4. (英) Aorta, Thoracic
5. (英) Atherosclerosis
6. (英) Coronary Vessels
7. (英) Disease Models, Animal
8. (英) Lipid Peroxidation
9. (英) MAP Kinase Kinase 4
10. (英) Male
11. (英) Mice
12. (英) Mice, Inbred C57BL
13. (英) Mice, Knockout
14. (英) Nitric Oxide
15. (英) Proto-Oncogene Proteins c-akt
16. (英) Receptor, Angiotensin, Type 1
17. (英) Receptor, Angiotensin, Type 2
18. (英) Receptors, Androgen
19. (英) Superoxides
20. (英) Thiobarbituric Acid Reactive Substances
21. (英) Transforming Growth Factor beta1
22. (英) Vasoconstrictor Agents

1. (英) Article.Affiliation: Department of Medicine and Bioregulatory Sciences, University of Tokushima Graduate School of Health Biosciences, Tokushima, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't