Abstract
It has been well confirmed ox-LDL plays key roles in the development of atherosclerosis via binding to LOX-1 and inducing apoptosis in vascular endothelial cells. Recent studies have shown ox-LDL can suppress microRNA has-let-7g, which in turn inhibits the ox-LDL induced apoptosis. However, details need to be uncovered. To determine the anti-atherosclerosis effect of microRNA has-let-7g, and to evaluate the possibility of CASP3 as an anti-atherosclerotic drug target by has-let-7g, the present study determined the role of hsa-let-7g miRNA in ox-LDL induced apoptosis in the vascular endothelial cells. We found that miRNA has-let-7g was suppressed during the ox-LDL-induced apoptosis in EAhy926 endothelial cells. In addition, overexpression of has-let-7g negatively regulated apoptosis in the endothelial cells by targeting caspase-3 expression. Therefore, miRNA let-7g may play important role in endothelial apoptosis and atherosclerosis.
Highlights
It has been well confirmed of key roles of oxidized low-density lipoprotein in the development of atherosclerosis [1] Endothelial cells, macrophages, and smooth muscle cells, which are involved in atherosclerosis, exhibit atherosclerotic alterations, post exposing to ox-LDL in vitro [2].Int
The ox-LDL can upregulate in endothelial cells, the LOX-1 expression, which can be induced by cytokine tumor necrosis factor-α (TNF-α) [6], and angiotensin II [7] as well
Ox-LDL-induced apoptosis has been reported in various cell models, i.e., vascular endothelial cells [4,8] and vascular smooth muscle cells [9], and it was further determined whether the decreased EAhy926 cell viability was caused by apoptosis
Summary
It has been well confirmed of key roles of oxidized low-density lipoprotein (ox-LDL) in the development of atherosclerosis [1] Endothelial cells, macrophages, and smooth muscle cells, which are involved in atherosclerosis, exhibit atherosclerotic alterations, post exposing to ox-LDL in vitro [2]. Ox-LDL is known to induce apoptosis, monocyte adhesion, and reactive oxygen species generation [3,4,5]. Via binding to the lectin-like endothelial ox-LDL receptor (LOX-1) [4] on the vascular endothelial cells. The ox-LDL can upregulate in endothelial cells, the LOX-1 expression, which can be induced by cytokine tumor necrosis factor-α (TNF-α) [6], and angiotensin II [7] as well
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
