• Xinming Zhou, Yongguang Xiao, Zhifu Mao, Jie Huang, Qing Geng, Wei Wang, and Ping Dong.
• Department of Thoracic Surgery, People's Hospital of New District Longhua, Jianshedong Road, Longhua, Shenzhen, Guangzhou Province 518109, China. Electronic address: zhouxm0101@163.com.
• Microvasc. Res. 2015 Jul 1; 100: 9-16.

AbstractThe excessive proliferation of vascular smooth muscle cells was key factor in the restenosis of vein graft. And the Notch signaling was demonstrated to regulate vSMC proliferation and differentiation. Soluble Jagged-1 (sJag1) can inhibit Notch signaling in vitro and in vivo; however, its capacity to suppress restenosis of vein graft remains unknown. Under the microscope, the left jugular vein of these rats was interposed into the left common carotid artery, followed without any treatment (control), or with Ad-Jag1 (treatment) or placebo (DMSO) post operation. We showed that Ad-Jag1 can attenuate restenosis of vein graft by inducing decreased proliferation and increased apoptosis in vivo. Notch1-Hey2 signaling is critical for the development of intima thickening by controlling vSMC-fate determination. By blocking Notch signaling, Ad-Jag1 can significantly inhibit intima thickening. These studies identify that Ad-Jag1 can restore the vSMC phenotype and inhibit the vSMC proliferation by suppression of Notch1 signaling, and thus open a new avenue for the treatment of restenosis in vein graft.Copyright © 2015 Elsevier Inc. All rights reserved.

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