You B, Yan G, Chen S, Sun J. The nuclear orphan receptor Nur77 suppresses endothelial cell activation through induction of IkappaB expression. Circulation Research, 2009; 104 (6):742-9.

Endothelial inflammation plays a critical role in the development and progression of cardiovascular disease. We demonstrate that orphan nuclear receptor Nur77 negatively regulates the TNF-alpha- and interleukin-1beta-induced vascular EC activation by transcriptionally upregulation of IkappaBalpha expression.

Li P, Zhu N, Yi B, Wang N, Chen M, You X, Zhao X, Slolomides CC, Qin Y, Sun J. MicroRNA-663 Regulates Human Vascular Smooth Muscle Cell Phenotypic Switch and Vascular Neointimal Formation. Circulation Research, 2013; 113(10):1117-27. 

Abnormal phenotypic switch of vascular smooth muscle cell (VSMC) is a hallmark of vascular disorders such as atherosclerosis and restenosis after angioplasty. We identify miR-663 as a novel modulator of human VSMC phenotypic switch by targeting JunB/myosin light chain 9 expression. Our results suggest that targeting miR-663 or its specific downstream targets in human VSMCs may represent an attractive approach for the treatment of proliferative vascular diseases.

Yang P, Wei X, Zhang J, Yi B, Zhang GX, Yin L, Yang XF, Sun J. Antithrombotic Effects of Nur77 and Nor1 Are Mediated Through Upregulating Thrombomodulin Expression in Endothelial Cells. Arterioscler Thromb Vasc Biol, 2016;36(2):361-9. 

Thrombomodulin is highly expressed on the lumenal surface of vascular endothelial cells (ECs) and possesses potent anticoagulant, antifibrinolytic, and anti-inflammatory activities in the vessel wall. We identify nuclear receptor Nur77 and Nor1 as novel regulators of thrombomodulin expression and function in vascular ECs and provide a proof-of-concept demonstration that targeted increasing expression of Nur77 and Nor1 in the vascular endothelium might represent a novel therapeutic approach for the treatment of thrombotic disorders.

Chen J, Zhang J, Shaik NF, Yi B, Wei X, Yang XF, Naik UP, Summer R, Yan G, Xu X, Sun J. The histone deacetylase inhibitor tubacin mitigates endothelial dysfunction by up-regulating the expression of endothelial nitric oxide synthase. J Biol Chem. 2019;294 (51):19565-19576. 

Endothelial nitric oxide (NO) synthase (eNOS) plays a critical role in the maintenance of blood vessel homeostasis. Our findings demonstrate that HDAC6 inhibitor tubacin exhibits potent eNOS-inducing effects and suggest that this compound might be useful for the prevention or management of endothelial dysfunction-associated cardiovascular diseases.