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Molecular Mechanisms of Nitric Oxide in Human Diseases
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Molecular Mechanisms of Nitric Oxide in Human Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2019) | Viewed by 19269

Special Issue Editors

Dr. Pandu Gangula

E-Mail Website
Guest Editor
Department of ODS and Research, School of Dentistry, Meharry Medical College, Nashville, TN 37208, USA
Interests: nitric oxide; GI motility; oral and systemic connection; vascular neuropeptides; Nrf2
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Robert Garfield

E-Mail Website
Guest Editor
Department of Ob/Gyn, College of Medicine, University of Arizona, Phoenix, AZ 85721, USA
Interests: obstetrics & gynecology; function of the uterus and cervix; preterm labor/birth
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nitric oxide (NO) is a ubiquitous, water-soluble and free radical gas, which plays an integral role in every cell function of all organs. Knowing the potential role of NO as a therapeutic compound in health and disease, a great of emphasis has been given to understanding the molecular and sources of NO production; including upstream (NO synthases, cofactor activities) and downstream cGMP-PKG-PDE5 and nitrate-nitrite-NO pathways. In addition, a role of microbiome on NO regulation has been investigated recently. In contrast, uncoupling of NOS due to lack of cofactors could lead to the formation of peroxynitrate and overproduction of reactive oxygen species (ROS) that could damage the cellular and organ functions. Therefore, a balance between NO and antioxidant synthesis is critical in maintaining normal physiological function.

This Special Issue, “Molecular Mechanisms of Nitric Oxide in Health and Disease”, will cover a selection of recent research topics and current review articles in the field of nitric oxide signaling and its role in various health outcomes. We solicit your participation and invite you to submit manuscripts. Experimental and bioinformatics papers, up-to-date review articles, and commentaries are also welcome.

Prof. Dr. Pandu Gangula
Prof. Dr. Robert Garfield
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • NOS
  • NO donors
  • Chronic Diseases
  • Microbiome
  • Oxidative Stress
  • Antioxidants
  • Estrogen
  • Progesterone

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Published Papers (4 papers)

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Research

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15 pages, 2311 KiB  
Article
The Selective Acetamidine-Based iNOS Inhibitor CM544 Reduces Glioma Cell Proliferation by Enhancing PARP-1 Cleavage In Vitro
by Marialucia Gallorini, Cristina Maccallini, Alessandra Ammazzalorso, Pasquale Amoia, Barbara De Filippis, Marialuigia Fantacuzzi, Letizia Giampietro, Amelia Cataldi and Rosa Amoroso
Int. J. Mol. Sci. 2019, 20(3), 495; https://doi.org/10.3390/ijms20030495 - 24 Jan 2019
Cited by 16 | Viewed by 3894
Abstract
Gliomas are the most aggressive adult primary brain tumors. Expression of inducible Nitric Oxide Synthase has been reported as a hallmark of chemoresistance in gliomas and several studies have reported that inhibition of inducible Nitric Oxide Synthase could be related to a decreased [...] Read more.
Gliomas are the most aggressive adult primary brain tumors. Expression of inducible Nitric Oxide Synthase has been reported as a hallmark of chemoresistance in gliomas and several studies have reported that inhibition of inducible Nitric Oxide Synthase could be related to a decreased proliferation of glioma cells. The present work was to analyze the molecular effects of the acetamidine derivative compound 39 (formally CM544, N-(3-{[(1-iminioethyl)amino]methyl}benzyl) prolinamide dihydrochloride), a newly synthetized iNOS inhibitor, in a C6 rat glioma cell model. There is evidence of CM544 selective binding to the iNOS, an event that triggers the accumulation of ROS/RNS, the expression of Nrf-2 and the phosphorylation of MAPKs after 3 h of treatment. In the long run, CM544 leads to the dephosphorylation of p38 and to a massive cleavage of PARP-1, confirming the block of C6 rat glioma cell proliferation in the G1/S checkpoint and the occurrence of necrotic cell death. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Nitric Oxide in Human Diseases)
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17 pages, 5866 KiB  
Article
Ginsenoside Rb1 Blocks Ritonavir-Induced Oxidative Stress and eNOS Downregulation through Activation of Estrogen Receptor-Beta and Upregulation of SOD in Human Endothelial Cells
by Jian-Ming Lü, Jun Jiang, Md Saha Jamaluddin, Zhengdong Liang, Qizhi Yao and Changyi Chen
Int. J. Mol. Sci. 2019, 20(2), 294; https://doi.org/10.3390/ijms20020294 - 12 Jan 2019
Cited by 34 | Viewed by 4947
Abstract
We have previously shown that ritonavir (RTV), a highly active anti-retroviral therapy (HAART) drug, can cause endothelial dysfunction through oxidative stress. Several antioxidants including ginsenoside Rb1, a compound with antioxidant effect, can effectively block this side effect of RTV in endothelial cells. In [...] Read more.
We have previously shown that ritonavir (RTV), a highly active anti-retroviral therapy (HAART) drug, can cause endothelial dysfunction through oxidative stress. Several antioxidants including ginsenoside Rb1, a compound with antioxidant effect, can effectively block this side effect of RTV in endothelial cells. In the current study, we explored a mechanism by which ginsenoside Rb1 could protect these cells via binding of estrogen receptors (ERs). We found that several human endothelial cell lines differentially expressed ER-β and had very low levels of ER-α. RTV treatment significantly increased the production of reactive oxygen species (ROS) and decreased the expression of endothelial nitric oxidase synthase (eNOS) and superoxide dismutase (SOD) in HUVECs, while Rb1 effectively blocked these effects of RTV. These effects of Rb1 were effectively inhibited by silencing ER-β, indicating that ginsenoside Rb1 requires ER-β for its antioxidant activity in inhibiting the deleterious effect of RTV in human endothelial cells. Furthermore, Rb1 specifically activated ER-β transactivation activity by ER-β luciferase reporter assay. Rb1 competitively bound to ER-β, which was determined by the high sensitive fluorescent polarization assay. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Nitric Oxide in Human Diseases)
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Review

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14 pages, 1002 KiB  
Review
The Role of Nitric Oxide in Regulating Intestinal Redox Status and Intestinal Epithelial Cell Functionality
by Kaiwen Mu, Shengwu Yu and David D. Kitts
Int. J. Mol. Sci. 2019, 20(7), 1755; https://doi.org/10.3390/ijms20071755 - 9 Apr 2019
Cited by 49 | Viewed by 5885
Abstract
Important functions of intestinal epithelial cells (IECs) include enabling nutrient absorption to occur passively and acting as a defense barrier against potential xenobiotic components and pathogens. A compromise to IEC function can result in the translocation of bacteria, toxins, and allergens that lead [...] Read more.
Important functions of intestinal epithelial cells (IECs) include enabling nutrient absorption to occur passively and acting as a defense barrier against potential xenobiotic components and pathogens. A compromise to IEC function can result in the translocation of bacteria, toxins, and allergens that lead to the onset of disease. Thus, the maintenance and optimal function of IECs are critically important to ensure health. Endogenous biosynthesis of nitric oxide (NO) regulates IEC functionality both directly, through free radical activity, and indirectly through cell signaling mechanisms that impact tight junction protein expression. In this paper, we review the current knowledge on factors that regulate inducible nitric oxide synthase (iNOS) and the subsequent roles that NO has on maintaining IECs’ intestinal epithelial barrier structure, functions, and associated mechanisms of action. We also summarize important findings on the effects of bioactive dietary food components that interact with NO production and affect downstream intestinal epithelium integrity. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Nitric Oxide in Human Diseases)
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12 pages, 753 KiB  
Review
Changes in Endothelial Nitric Oxide Production in Systemic Vessels during Early Ontogenesis—A Key Mechanism for the Perinatal Adaptation of the Circulatory System
by Dina K. Gaynullina, Rudolf Schubert and Olga S. Tarasova
Int. J. Mol. Sci. 2019, 20(6), 1421; https://doi.org/10.3390/ijms20061421 - 21 Mar 2019
Cited by 28 | Viewed by 3930
Abstract
Nitric oxide (NO) produced in the wall of blood vessels is necessary for the regulation of vascular tone to ensure an adequate blood supply of organs and tissues. In this review, we present evidence that the functioning of endothelial NO-synthase (eNOS) changes considerably [...] Read more.
Nitric oxide (NO) produced in the wall of blood vessels is necessary for the regulation of vascular tone to ensure an adequate blood supply of organs and tissues. In this review, we present evidence that the functioning of endothelial NO-synthase (eNOS) changes considerably during postnatal maturation. Alterations in NO-ergic vasoregulation in early ontogeny vary between vascular beds and correlate with the functional reorganization of a particular organ. Importantly, the anticontractile effect of NO can be an important mechanism responsible for the protectively low blood pressure in the immature circulatory system. The activity of eNOS is regulated by a number of hormones, including thyroid hormones which are key regulators of the perinatal developmental processes. Maternal thyroid hormone deficiency suppresses the anticontractile effect of NO at perinatal age. Such alterations disturb perinatal cardiovascular homeostasis and lead to delayed occurring cardiovascular pathologies in adulthood. The newly discovered role of thyroid hormones may have broad implications in cardiovascular medicine, considering the extremely high prevalence of maternal hypothyroidism in human society. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Nitric Oxide in Human Diseases)
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