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Nitric Oxide Synthases: Function and Regulation 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 20 July 2024 | Viewed by 2056

Special Issue Editor


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Guest Editor
Graduate Institute, Department of Physiology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan
Interests: cell culture; cholesterol metabolism; atherosclerosis; reactive oxygen species; signaling; endothelial cell biology; endothelial dysfunction; angiogenesis; vascular biology; vascular diseases; macrophage-foam cells; cardiovascular physiology
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Nitric Oxide Synthases: Function and Regulation”.

Nitric oxide (NO) is a bioactive gas in the body that 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 types of cell. 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. This Special Issue of IJMS aims to provide a research platform to host a collection of the latest review and original research articles covering all aspects of these enzymes.

Prof. Dr. Tzong-Shyuan Lee
Guest Editor

Manuscript Submission Information

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Keywords

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

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Published Papers (2 papers)

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Research

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17 pages, 5807 KiB  
Article
Cinnamaldehyde Protects against P. gingivalis Induced Intestinal Epithelial Barrier Dysfunction in IEC-6 Cells via the PI3K/Akt-Mediated NO/Nrf2 Signaling Pathway
by Chethan Sampath, Sasanka S. Chukkapalli, Abhinav V. Raju, Leela Subhashini C. Alluri, Dollada Srisai and Pandu R. Gangula
Int. J. Mol. Sci. 2024, 25(9), 4734; https://doi.org/10.3390/ijms25094734 - 26 Apr 2024
Viewed by 284
Abstract
Porphyromonas gingivalis (Pg), a Gram-negative oral pathogen, promotes and accelerates periodontitis-associated gut disorders. Intestinal epithelial barrier dysfunction is crucial in the pathogenesis of intestinal and systemic diseases. In this study, we sought to elucidate the protective role of cinnamaldehyde (CNM, an [...] Read more.
Porphyromonas gingivalis (Pg), a Gram-negative oral pathogen, promotes and accelerates periodontitis-associated gut disorders. Intestinal epithelial barrier dysfunction is crucial in the pathogenesis of intestinal and systemic diseases. In this study, we sought to elucidate the protective role of cinnamaldehyde (CNM, an activator of Nrf2) against P. gingivalis (W83) and Pg-derived lipopolysaccharide (Pg-LPS) induced intestinal epithelial barrier dysfunction via antioxidative mechanisms in IEC-6 cells. IEC-6 (ATCC, CRL-1592) cells were pretreated with or without CNM (100 µM), in the presence or absence of P. gingivalis (strain W83, 109 MOI) or Pg-LPS (1, 10, and 100 µg/mL), respectively, between 0–72 h time points by adopting a co-culture method. Intestinal barrier function, cytokine secretion, and intestinal oxidative stress protein markers were analyzed. P. gingivalis or Pg-LPS significantly (p < 0.05) increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels expressing oxidative stress damage. Pg-LPS, as well as Pg alone, induces inflammatory cytokines via TLR-4 signaling. Furthermore, infection reduced Nrf2 and NAD(P)H quinone dehydrogenase 1 (NQO1). Interestingly, inducible nitric oxide synthase (iNOS) protein expression significantly (p < 0.05) increased with Pg-LPS or Pg infection, with elevated levels of nitric oxide (NO). CNM treatment suppressed both Pg- and Pg-LPS-induced intestinal oxidative stress damage by reducing ROS, MDA, and NO production. Furthermore, CNM treatment significantly upregulated the expression of tight junction proteins via increasing the phosphorylation levels of PI3K/Akt/Nrf2 suppressing inflammatory cytokines. CNM protected against Pg infection-induced intestinal epithelial barrier dysfunction by activating the PI3K/Akt-mediated Nrf2 signaling pathway in IEC-6 cells. Full article
(This article belongs to the Special Issue Nitric Oxide Synthases: Function and Regulation 2.0)
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Review

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15 pages, 1553 KiB  
Review
The Physiological Function of nNOS-Associated CAPON Proteins and the Roles of CAPON in Diseases
by Wenshuo Xie, Nianhong Xing, Jicheng Qu, Dongwu Liu and Qiuxiang Pang
Int. J. Mol. Sci. 2023, 24(21), 15808; https://doi.org/10.3390/ijms242115808 - 31 Oct 2023
Cited by 1 | Viewed by 1208
Abstract
In this review, the structure, isoform, and physiological role of the carboxy-terminal PDZ ligand of neuronal nitric oxide synthase (CAPON) are summarized. There are three isoforms of CAPON in humans, including long CAPON protein (CAPON-L), short CAPON protein (CAPON-S), and CAPON-S’ protein. CAPON-L [...] Read more.
In this review, the structure, isoform, and physiological role of the carboxy-terminal PDZ ligand of neuronal nitric oxide synthase (CAPON) are summarized. There are three isoforms of CAPON in humans, including long CAPON protein (CAPON-L), short CAPON protein (CAPON-S), and CAPON-S’ protein. CAPON-L includes three functional regions: a C-terminal PDZ-binding motif, carboxypeptidase (CPE)-binding region, and N-terminal phosphotyrosine (PTB) structural domain. Both CAPON-S and CAPON-S’ only contain the C-terminal PDZ-binding motif. The C-terminal PDZ-binding motif of CAPON can bind with neuronal nitric oxide synthase (nNOS) and participates in regulating NO production and neuronal development. An overview is given on the relationship between CAPON and heart diseases, diabetes, psychiatric disorders, and tumors. This review will clarify future research directions on the signal pathways related to CAPON, which will be helpful for studying the regulatory mechanism of CAPON. CAPON may be used as a drug target, which will provide new ideas and solutions for treating human diseases. Full article
(This article belongs to the Special Issue Nitric Oxide Synthases: Function and Regulation 2.0)
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