التفاصيل البيبلوغرافية
| العنوان: |
High Salt Intake Worsens Aortic Dissection in Mice ; Involvement of IL (Interleukin)-17A–Dependent ECM (Extracellular Matrix) Metabolism |
| المؤلفون: |
Nishida, Norifumi, Aoki, Hiroki, Ohno-Urabe, Satoko, Nishihara, Michihide, Furusho, Aya, Hirakata, Saki, Hayashi, Makiko, Ito, Sohei, Yamada, Hiroshi, Hirata, Yuichiro, Yasukawa, Hideo, Imaizumi, Tsutomu, Tanaka, Hiroyuki, Fukumoto, Yoshihiro |
| المصدر: |
Arteriosclerosis, Thrombosis, and Vascular Biology ; volume 40, issue 1, page 189-205 ; ISSN 1079-5642 1524-4636 |
| بيانات النشر: |
Ovid Technologies (Wolters Kluwer Health) |
| سنة النشر: |
2020 |
| الوصف: |
Objective: Aortic dissection (AD) is a fatal disease that occurs suddenly without preceding clinical signs or symptoms. Although high salt intake is a proposed risk factor for cardiovascular diseases, the relationship between AD and high salt intake has not been clarified. We examined the effect of high-salt challenge on a mouse AD model. Approach and Results: AD was induced in male mice by continuous infusion of β-aminopropionitrile and Ang II (angiotensin II). High-salt challenge exacerbated aortic wall destruction in AD. Deletion of Il17a (IL-17KO [IL (interleukin)-17A knockout]) did not affect the AD phenotype at baseline, but it abolished the high salt–induced worsening of the aortic destruction. Unexpectedly, aortas of IL-17KO mice exhibited global changes in ECM (extracellular matrix)-related genes without alteration of proinflammatory genes, altered architecture of collagen fibers, and reduced stiffness before AD induction. The aortas of IL-17KO mice were less sensitive to AD-inducing stimuli, as shown by the induction of phenotypic modulation markers SMemb and vimentin, suggesting a reduced stress response. The aortas of IL-17KO mice had a higher population of smooth muscle cells with nuclear-localized phosphorylated Smad2, indicative of TGFβ (transforming growth factor-beta) signal activation. Consistently, pretreatment of smooth muscle cells in culture with IL-17A blunted the activation of Smad2 by TGFβ1. Conclusions: These findings indicate that high salt intake has a worsening effect on AD in the context of high aortic wall stiffness, which is under the control of IL-17A through ECM metabolism. Therefore, salt restriction may represent a low-cost and practical way to reduce AD risk. |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
English |
| DOI: |
10.1161/atvbaha.119.313336 |
| DOI: |
10.1161/ATVBAHA.119.313336 |
| الإتاحة: |
https://doi.org/10.1161/atvbaha.119.313336Test |
| رقم الانضمام: |
edsbas.DB86BBD |
| قاعدة البيانات: |
BASE |
