Open Access<p>Laquinimod Protects Against TNF-α-Induced Attachment of Monocytes to Human Aortic Endothelial Cells (HAECs) by Increasing the Expression of KLF2</p>
Author(s) -
Tiechao Jiang,
Wenhao Zhang,
Zhongyu Wang
Publication year - 2020
Publication title -
drug design, development and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.964
H-Index - 64
ISSN - 1177-8881
DOI - 10.2147/dddt.s243666
Subject(s) - klf2 , proinflammatory cytokine , medicine , chemokine , inflammation , endothelial dysfunction , western blot , immunology , tumor necrosis factor alpha , endothelium , immune system , microbiology and biotechnology , monocyte , chemistry , biology , biochemistry , gene expression , gene
As a worldwide health issue, the treatment and prevention of atherosclerosis present an important goal. Increased levels of proinflammatory cytokines such as TNF-α-associated chronic inflammatory response cause endothelial cells to lose their ability to regulate vascular function. Lipid-laden immune cells are recruited to the endothelium where they adhere to the endothelial wall and invade the intimal space, thereby leading to the development of atherosclerotic lesions, fatty plaques, and thickening of the arterial wall. In the present study, for the first time, we investigated the effects of laquinimod, an immunomodulatory agent used for the treatment of multiple sclerosis, on human aortic endothelial in a TNF-α-induced atherosclerotic microenvironment. At present, the mechanism of action of laquinimod is not well defined.