Theranostics 2019; 9(25):7961-7975. doi:10.7150/thno.35737 This issue

Research Paper

miR-27a regulates vascular remodeling by targeting endothelial cells' apoptosis and interaction with vascular smooth muscle cells in aortic dissection

Yudong Sun1,2*, Yu Xiao1*, Huiying Sun1, Zhiqing Zhao1, Jiang Zhu1, Lei Zhang1, Jian Dong1, Tonglei Han1, Qing Jing3, Jian Zhou1, Zaiping Jing1✉

1. Department of vascular surgery, Changhai Hospital, The Naval Military Medical University, Shanghai, China.
2. Depaertment of general surgery, Jingling Hospital, Medical School of Nanjing University, Nanjing, China
3. Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine (SJTUSM) & Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai 200025, China.
*These authors contributed equally to the study

This is an open access article distributed under the terms of the Creative Commons Attribution License ( See for full terms and conditions.
Sun Y, Xiao Y, Sun H, Zhao Z, Zhu J, Zhang L, Dong J, Han T, Jing Q, Zhou J, Jing Z. miR-27a regulates vascular remodeling by targeting endothelial cells' apoptosis and interaction with vascular smooth muscle cells in aortic dissection. Theranostics 2019; 9(25):7961-7975. doi:10.7150/thno.35737. Available from

File import instruction


Graphic abstract

Rationale: Aortic dissection (AD) is caused by functional disorder of cells in the aortic wall, which is largely attributed to vascular remodeling. Therapeutic strategies for AD remain limited due to our incomplete understanding of the role of endothelial cells (ECs) in AD pathogenesis. This study aimed to identify the regulatory role of miR-27a in AD and provide a mechanistic basis for a non-invasive treatment of AD.

Methods: We harvested aortas from normal and AD patients to explore the expression of miR-27a. In vitro and in vivo assays were preformed to explore the biological effects of differential expression of miR-27a in ECs and its regulatory effect on AD.

Results: MiR-27a was lower in intima of AD samples than in healthy individuals. Downregulation of miR-27a in EC was due to up-regulated expression of fas-associated protein with death domain (FADD) and the activation of apoptosis pathway, which led to apoptosis of ECs. Migration of vascular smooth muscle cells was promoted by EC after downregulation of miR-27a due to enhancement of growth/differentiation factor 8 (GDF8) and repression of matrix metalloproteinase-20 (MMP20) in the co-culture system supernatants. Increase in FADD and apoptosis of ECs to induce AD was shown using mouse models of AD in which miR-27a was stably knocked-down by antagomir. Up-regulation of miR-27a by agomir led to a protective effect on AD.

Conclusion: Treatment with miR-27a activator that targets apoptosis of ECs strongly diminished occurrence of AD, providing a new strategy for this disease.

Keywords: aortic dissection, miR-27a, endothelial cell, apoptosis, FADD