Estrogen regulation of nitric oxide and inducible nitric oxide synthase (iNOS) in immune cells: Implications for immunity, autoimmune diseases, and apoptosis

Karpuzoglu, Ebru; Ahmed, S. Ansar

doi:10.1016/j.niox.2006.03.009

Cited by 147 publications

(124 citation statements)

References 91 publications

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“…E 2 exerts many of its effects in cardiomyocytes through activation of the insulin receptor substrate 1 (IRS1), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) signalling cascades (Kypreos et al 2014, Obradovic et al 2014). E 2 exerts beneficial effects on the cardiovascular system by reducing nuclear factor kappa-B (NFkB), IkB and iNOS expression during ischemia (Karpuzoglu, Ahmed 2006). Under normal conditions, E 2 also influences energy usage by regulating GLUT and CD36 in heart (Gorres et al 2011, Tepavcevic et al 2011.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović

Obradović

Sudar-Milovanović

et al. 2017

Molecular and Cellular Endocrinology

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Please cite this article as: Zafirovic, S., Obradovic, M., Sudar-Milovanovic, E., Jovanovic, A., Stanimirovic, J., Stewart, A.J., Pitt, S.J., Isenovic, E.R., 17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats, Molecular and Cellular Endocrinology (2017), doi: 10.1016/j.mce.2017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe aim of this study was to investigate the in vivo effects of estradiol (E 2 ) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. MaleWistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E 2 while the other half were placebo-treated. 24h after treatment animals were sacrificed. E 2 reduced cardiac free fatty acid (FFA Akt, protein kinase B; AS160, Akt substrate of 160 kDa; CD36, fatty acid transporters; E 2 ,

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović

Obradović

Sudar-Milovanović

et al. 2017

Molecular and Cellular Endocrinology

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“…There was a marked acute inflammatory response characterized by neutrophil influx peaking at 1 dpi but much greater than in pH1N1 infection, with a neutrophil count that was nearly twice as high (Figure 9). This could be explained by a higher induction of pro-inflammatory cytokine production (e.g., IL-6 and IL-8) and NO production due to H5N1 infection [22,23]. Maines et al [10] demonstrated a relatively high production of IL-6 and IL-8 in the lower respiratory tract of ferrets infected with H5N1, but not with pH1N1.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Temporal and Spatial Dynamics of Seasonal H3N2, Pandemic H1N1 and Highly Pathogenic avian influenza H5N1 Virus Infections in Ferrets

Brand

Stittelaar

Amerongen

et al. 2013

Journal of Comparative Pathology

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Humans may be infected by different influenza A viruses-seasonal, pandemic, and zoonotic-which differ in presentation from mild upper respiratory tract disease to severe and sometimes fatal pneumonia with extra-respiratory spread. Differences in spatial and temporal dynamics of these infections are poorly understood. Therefore, we inoculated ferrets with seasonal H3N2, pandemic H1N1 (pH1N1), and highly pathogenic avian H5N1 influenza virus and performed detailed virological and pathological analyses at time points from 0.5 to 14 days post inoculation (dpi), as well as describing clinical signs and hematological parameters. H3N2 infection was restricted to the nose and peaked at 1 dpi. pH1N1 infection also peaked at 1 dpi, but occurred at similar levels throughout the respiratory tract. H5N1 infection occurred predominantly in the alveoli, where it peaked for a longer period, from 1 to 3 dpi. The associated lesions followed the same spatial distribution as virus infection, but their severity peaked between 1 and 6 days later. Neutrophil and monocyte counts in peripheral blood correlated with inflammatory cell influx in the alveoli. Of the different parameters used to measure lower respiratory tract disease, relative lung weight and affected lung tissue allowed the best quantitative distinction between the virus groups. There was extra-respiratory spread to more tissues-including the central nervous system-for H5N1 infection than for pH1N1 infection, and to none for H3N2 infection. This study shows that seasonal, pandemic, and zoonotic influenza viruses differ strongly in the spatial and temporal dynamics of infection in the respiratory tract and extra-respiratory tissues of ferrets.

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“…Neuronal NOS (NOS-1 or nNOS) and endothelial NOS (NOS-3 or eNOS, studied in this manuscript) require calcium/calmodulin for activation to produce a continuous basal release of NO [20,21]. The third isoform is a calcium-independent, inducible form (iNOS or NOS-2), which is expressed in response to pro-inflammatory cytokines [22]. Apart from calcium, several other factors can regulate the activity of the NOS isoforms.…”

Section: Discussionmentioning

confidence: 99%

Regulation of the nitric oxide pathway genes by tetrahydrofurandiols: Microarray analysis of MCF-7 human breast cancer cells

et al. 2008

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THF-diols (9,12-oxy-10,13-dihydroxyoctadecanoic and 10,13-oxy-9,12-dihydroxyoctadecanoic acids) are endocrine disrupters in rats and mitogens in breast cancer cells. Microarray analyses and real-time PCR analyses on RNA from THF-treated MCF-7 cells revealed a number of genes (Caveolin 1, Heat Shock Protein 90α and 90β, vascular endothelial growth factor, ATPase, Ca++ transporting, ubiquitous) in the Nitric Oxide Pathway (NOP) were targets for THF-diols. Chromatin immunoprecipitation studies suggest THF-diols modify of histone H4 acetylation at the Caveolin 1 promoter via an epigenetic mechanism. These findings are consistent with the well-known involvement of NOP genes in cell proliferation and sexual behavior.

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Estrogen regulation of nitric oxide and inducible nitric oxide synthase (iNOS) in immune cells: Implications for immunity, autoimmune diseases, and apoptosis

Cited by 147 publications

References 91 publications

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Comparison of Temporal and Spatial Dynamics of Seasonal H3N2, Pandemic H1N1 and Highly Pathogenic avian influenza H5N1 Virus Infections in Ferrets

Regulation of the nitric oxide pathway genes by tetrahydrofurandiols: Microarray analysis of MCF-7 human breast cancer cells

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