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Dear Colleagues,

Nitric oxide (NO) is a bioactive gas in the body and plays a crucial role in maintaining the homeostasis of the cardiovascular system. It can be synthesized by endothelial nitric oxide synthase (eNOS), neuronal NO synthase (nNOS), and inducible NO synthase (iNOS), which convert arginine into citrulline and produce NO in several cell types. In addition to its key role in regulating the cardiovascular function, NO has been reported to be involved in the pathological processes of a variety of human diseases, including cardiovascular diseases, metabolic diseases, inflammatory diseases, cancer, and neurological diseases. Given the importance of NOSs in the pathophysiology of human diseases, these enzymes are considered potential therapeutic targets for the treatment of diverse human pathologies. The Special Issue entitled "Nitric Oxide Synthases: Regulation and Function" aims to provide a research platform for the collection of the latest review and original research articles covering all aspects of these enzymes.

Prof. Dr. Tzong-Shyuan Lee
Guest Editor

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Keywords

NOSs
nitric oxide synthases
isoforms
nitric oxide
endothelial cell
stem cell
cellular signaling
redox pathway
endothelial NOS
neuronal NOS
disease
cancer

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17 pages, 4835 KiB

Open AccessArticle

Endothelial Nitric Oxide Mediates the Anti-Atherosclerotic Action of Torenia concolor Lindley var. Formosama Yamazaki

by Li-Ching Cheng, Bei-Chia Guo, Chia-Hui Chen, Chi-Jen Chang, Ta-Sen Yeh and Tzong-Shyuan Lee

Int. J. Mol. Sci. 2020, 21(4), 1532; https://doi.org/10.3390/ijms21041532 - 24 Feb 2020

Cited by 7 | Viewed by 3567

Abstract

Torenia concolor Lindley var. formosama Yamazaki ethanolic extract (TCEE) is reported to have anti-inflammatory and anti-obesity properties. However, the effects of TCEE and its underlying mechanisms in the activation of endothelial nitric oxide synthase (eNOS) have not yet been investigated. Increasing the endothelium-derived nitric oxide (NO) production has been known to be beneficial against the development of cardiovascular diseases. In this study, we investigated the effect of TCEE on eNOS activation and NO-related endothelial function and inflammation by using an in vitro system. In endothelial cells (ECs), TCEE increased NO production in a concentration-dependent manner without affecting the expression of eNOS. In addition, TCEE increased the phosphorylation of eNOS at serine 635 residue (Ser635) and Ser1179, Akt at Ser473, calmodulin kinase II (CaMKII) at threonine residue 286 (Thr286), and AMP-activated protein kinase (AMPK) at Thr172. Moreover, TCEE-induced NO production, and EC proliferation, migration, and tube formation were diminished by pretreatment with LY294002 (an Akt inhibitor), KN62 (a CaMKII inhibitor), and compound C (an AMPK inhibitor). Additionally, TCEE attenuated the tumor necrosis factor-α-induced inflammatory response as evidenced by the expression of adhesion molecules in ECs and monocyte adhesion onto ECs. These inflammatory effects of TCEE were abolished by L-NG-nitroarginine methyl ester (an NOS inhibitor). Moreover, chronic treatment with TCEE attenuated hyperlipidemia, systemic and aortic inflammatory response, and the atherosclerotic lesions in apolipoprotein E-deficient mice. Collectively, our findings suggest that TCEE may confer protection from atherosclerosis by preventing endothelial dysfunction. Full article

(This article belongs to the Special Issue Nitric Oxide Synthases: Regulation and Function 2.0)

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