ID | 116725 |
Title Alternative | Role of Sirt7 in Neointimal Formation
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Author |
Kimura, Yuichi
Kumamoto University
Izumiya, Yasuhiro
Osaka City University
Araki, Satoshi
Kumamoto University
Yamamura, Satoru
Kumamoto University
Hanatani, Shinsuke
Kumamoto University
Onoue, Yoshiro
Kumamoto University
Ishida, Toshifumi
Kumamoto University
Arima, Yuichiro
Kumamoto University
Nakamura, Taishi
Kumamoto University
Yamamoto, Eiichiro
Kumamoto University
Senokuchi, Takafumi
Kumamoto University
Yoshizawa, Tatsuya
Kumamoto University
Sata, Masataka
Tokushima University
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Kim-Mitsuyama, Shokei
Kumamoto University
Nakagata, Naomi
Kumamoto University
Bober, Eva
Max-Planck-Institute for Heart and Lung Research
Braun, Thomas
Max-Planck-Institute for Heart and Lung Research
Kaikita, Koichi
Kumamoto University
Yamagata, Kazuya
Kumamoto University
Tsujita, Kenichi
Kumamoto University
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Keywords | Neointimal formation
Sirtuin
Smooth muscle cell
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Content Type |
Journal Article
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Description | Background: Sirt7 is a recently identified sirtuin and has important roles in various pathological conditions, including cancer progression and metabolic disorders. It has previously been reported that Sirt7 is a key molecule in acute myocardial wound healing and pressure overload-induced cardiac hypertrophy. In this study, the role of Sirt7 in neointimal formation after vascular injury is investigated.
Methods and Results: Systemic (Sirt7−/−) and smooth muscle cell-specific Sirt7-deficient mice were subjected to femoral artery wire injury. Primary vascular smooth muscle cells (VSMCs) were isolated from the aorta of wild type (WT) and Sirt7−/−mice and their capacity for cell proliferation and migration was compared. Sirt7 expression was increased in vascular tissue at the sites of injury. Sirt7−/−mice demonstrated significant reduction in neointimal formation compared to WT mice. In vitro, Sirt7 deficiency attenuated the proliferation of serum-induced VSMCs. Serum stimulation-induced upregulation of cyclins and cyclin-dependent-kinase 2 (CDK2) was significantly attenuated in VSMCs of Sirt7−/−compared with WT mice. These changes were accompanied by enhanced expression of the microRNA 290-295 cluster, the translational negative regulator of CDK2, in VSMCs of Sirt7−/−mice. It was confirmed that smooth muscle cell-specific Sirt7-deficient mice showed significant reduction in neointima compared with control mice. Conclusions: Sirt7 deficiency attenuates neointimal formation after vascular injury. Given the predominant role in vascular neointimal formation, Sirt7 is a potentially suitable target for treatment of vascular diseases. |
Journal Title |
Circulation Journal
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ISSN | 13474820
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Publisher | The Japanese Circulation Society
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Volume | 85
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Issue | 12
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Start Page | 2232
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End Page | 2240
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Published Date | 2021-11-25
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Rights | This article is licensed under a Creative Commons [Attribution-NonCommercial-NoDerivatives 4.0 International] license. https://creativecommons.org/licenses/by-nc-nd/4.0/
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language |
eng
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Publisher
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departments |
Medical Sciences
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