ArticleInternational journal of clinical and experimental pathology2017
Soluble epoxide hydrolase inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid, represses human aortic smooth muscle cell proliferation and migration by regulating cell death pathways via the mTOR signaling.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- TPPU protects against seizures and seizure-associated comorbidities by inhibiting the Akt/mTOR signaling pathway in KA-induced convulsant mice.Frontiers in immunology · 2026Article
- Green synthesis of new chiral amino acid urea derivatives and evaluation of their anti-inflammatory activity.RSC advances · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
The soluble epoxide hydrolase (sEH) is a molecule necessary for the metabolism of endogenous constituents implicated in blood pressure regulation and vascular inflammation. Scientific evidences indicate that sEH inhibitors such as 12-(3-Adamantan-1-yl-ureido)-dodecanoic acid (AUDA) could be a possible therapeutic option for cardiovascular diseases such as restenosis and atherosclerosis. However, the nature of the biological effects of AUDA still remains unclear. Herein, we intended to scrutinize the influence of AUDA on proliferation and migration of TNF-α-induced human aortic smooth muscle cells (HASMCs) and the underlying molecular mechanism. Pretreatment with AUDA (0.5-8 µM) dose-dependently inhibited TNF-α-induced proliferation of HASMCs as revealed by the MTT assay and the decreased expression of Cyclin D1 and β-tubulin. Transwell analyses showed that AUDA equally suppressed TNF-α-induced migration of HASMCs. Moreover, AUDA induced the expression of apoptotic proteins (Caspase 3, PARP) and inhibited the expression of autophagy related markers (LC3-II and Beclin 1). More interestingly, AUDA inhibited TNF-α-induced phosphorylation of mTOR, the silencing of which abolished the inhibitory effects of AUDA on TNF-α-induced HASMCs. The present results point toward an inhibitory effect of AUDA on the proliferation and migration of TNF-α-induced HASMCs by regulation of cell death related signaling pathways via downregulation of the mTOR signaling. Thus, AUDA may be an important regulator of inflammation in the atherosclerotic lesion and a novel therapeutic drug for the treatment of atherosclerosis, restenosis and other cardiovascular diseases.
Indexed as
Identifiers
31966695PMC6965454W3012281752What OpenQuestion holds
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