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Published on: June 11, 2017
Sirt7 Deficiency Attenuates Neointimal Formation Following Vascular Injury by Modulating Vascular Smooth Muscle Cell
Yuichi Kimura1, Yasuhiro Izumiya2, Satoshi Araki1
1Department of Cardiovascular Medicine, Faculty of Life Sciences, Kumamoto University.
Sirtuin 7 (Sirt7) deficiency reduces neointimal formation after vascular injury by inhibiting smooth muscle cell proliferation and migration. This suggests Sirt7 is a potential therapeutic target for vascular diseases.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Vascular Biology
Background:
- Sirtuin 7 (Sirt7) is a sirtuin involved in cancer and metabolic disorders.
- Sirt7 plays a role in cardiac wound healing and hypertrophy.
- This study investigates Sirt7's role in neointimal formation post-vascular injury.
Purpose of the Study:
- To investigate the role of Sirtuin 7 (Sirt7) in neointimal hyperplasia following vascular injury.
- To determine if Sirt7 deficiency impacts vascular smooth muscle cell (VSMC) proliferation and migration.
Main Methods:
- Used systemic and smooth muscle cell-specific Sirt7-deficient mice subjected to femoral artery wire injury.
- Compared proliferation and migration of primary VSMCs from wild-type and Sirt7-deficient mice.
- Analyzed expression of cyclins, cyclin-dependent-kinase 2 (CDK2), and microRNA 290-295 cluster.
Main Results:
- Sirt7 expression increased at injury sites.
- Sirt7-deficient mice showed significantly reduced neointimal formation.
- Sirt7 deficiency attenuated VSMC proliferation and migration in vitro.
- Reduced CDK2 upregulation and enhanced microRNA 290-295 cluster expression were observed in Sirt7-deficient VSMCs.
Conclusions:
- Sirtuin 7 (Sirt7) deficiency attenuates neointimal formation after vascular injury.
- Sirt7 plays a significant role in vascular neointimal formation.
- Sirt7 is a potential therapeutic target for vascular diseases.
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