High expression of ubiquitin-specific peptidase 39 is associated with the development of vascular remodeling

He,Shuai; Zhong,Wei; Yin,Li; Wang,Yifei; Qiu,Zhibing; Song,Gang

doi:10.3892/mmr.2017.6297

High expression of ubiquitin-specific peptidase 39 is associated with the development of vascular remodeling

Authors:
- Shuai He
- Wei Zhong
- Li Yin
- Yifei Wang
- Zhibing Qiu
- Gang Song
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Affiliations: Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China, Cancer Research Center, Medical College of Xiamen University, Xiamen, Fujian 361102, P.R. China
Published online on: March 8, 2017 https://doi.org/10.3892/mmr.2017.6297
Pages: 2567-2573
Copyright: © He et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Vascular remodeling is the primary cause underlying the failure of angioplasty surgeries, including vascular stenting, transplant vasculopathy and vein grafts. Multiple restenosis‑associated proteins and genes have been identified to account for this. In the present study, the functions of ubiquitin‑specific peptidase 39 (USP39) were investigated in the context of two vascular remodeling models (a mouse common carotid artery ligation and a pig bilateral saphenous vein‑carotid artery interposition graft). USP39 has previously been observed to be upregulated in ligated arteries, and this result was confirmed in the pig vein graft model. In addition, Transwell assay results demonstrated that vascular smooth muscle cell (VSMC) migration was suppressed by lentiviral vector‑mediated downregulation of USP39 and enhanced by upregulation of USP39. Furthermore, knockdown of USP39 inhibited VSMC cell proliferation and the expression of cyclin D1 and cyclin‑dependent kinase 4, as analyzed via cell counting, MTT assay and western blotting. These results suggest that USP39 may represent a novel therapeutic target for treating vascular injury and preventing vein-graft failure.

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