Nitric Oxide Donor <scp>s</scp>‐Nitroso‐<scp>n</scp>‐Acetyl Penicillamine (SNAP) Alters Meiotic Spindle Morphogenesis in <i>Xenopus</i> Oocytes

Gelaude, Armance; Marin, Matthieu; Cailliau, Katia; Ješeta, Michal; Lescuyer‐Rousseau, Arlette; Vandame, Pauline; Nevoral, Jan; Sedmı́ková, Markéta; Martoriati, Alain; Bodart, Jean‐François

doi:10.1002/jcb.25211

Cited by 8 publications

(8 citation statements)

References 55 publications

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“…SNAP hindered the all-or-none response of MPF and MAPK pathways, especially in Xenopus oocytes; most oocytes exhibited partially active MPF and MAPK in the absence of any external signs of meiotic resumption [15]. Noticeably, SNAP altered meiotic spindle formation, therefore impairing proper genomic transmission [15]. This observation corroborates reports of mitosis inhibition through Tyrosine residue nitrosylation in plant models, and Alteration of cross walls orientation, presumably by impairing microtubules organization [16,17].…”

Section: No In Amphibian Oocytes Eggs and Embryossupporting

confidence: 78%

“…Under these conditions, SNAP lead heterogeneous response at the biochemical level with respect to the two pathways involved in meiotic resumption (MPF and MAPK). SNAP hindered the all-or-none response of MPF and MAPK pathways, especially in Xenopus oocytes; most oocytes exhibited partially active MPF and MAPK in the absence of any external signs of meiotic resumption [15]. Noticeably, SNAP altered meiotic spindle formation, therefore impairing proper genomic transmission [15].…”

Section: No In Amphibian Oocytes Eggs and Embryosmentioning

confidence: 99%

“…We would like to thank the personnel of the BICeL-Lille1-HB Facility for access to the microscopy systems and technical advices. We are indebted to the Research Federation FRABio for providing the scientific and technical environment to achieving our work [14,15]. MJ work in Department of Obstetrics and Gynaecology, Center of Assisted Reproduction, University Hospital Brno, and Masaryk University.…”

Section: Acknowledgementsmentioning

confidence: 99%

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From Nitric Oxide Toward S-Nitrosylation: Expanding Roles in Gametes and Embryos

Ješeta¹,

Sedmı́ková²,

Bodart³

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Nitric oxide (NO) is a gasotransmitter involved in various aspects of reproduction. The observational data from different species, such as sea urchin, ascidians, amphibians, rodents, porcine, bovine, and human, suggest that NO might have a significant role in reproduction through several mechanisms. This proposed role might appear preserved through evolution; however, the effects of NO also depend on the species or stages considered. There has been debate over the physiological relevance of NO, though the benefits of its use in assisted reproduction are now widely recognized. Over the past years, S-nitrosylation has provided a new angle to decipher the mechanisms through which NO exerts its actions. This chapter summarizes, in a nonexhaustive manner, research that explores the role of NO in gametes and embryos.

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Section: No In Amphibian Oocytes Eggs and Embryossupporting

confidence: 78%

Section: No In Amphibian Oocytes Eggs and Embryosmentioning

confidence: 99%

Section: Acknowledgementsmentioning

confidence: 99%

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From Nitric Oxide Toward S-Nitrosylation: Expanding Roles in Gametes and Embryos

Ješeta¹,

Sedmı́ková²,

Bodart³

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

Self Cite

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“…Low levels of nitric donors were utilized for the antigen presentation experiments. At concentrations 20 fold higher than utilized for the antigen presentation experiments, SNAP may generate free radicals and alter cellular microtubule organization 24 . In dog models, high concentrations of SNAP led to free radical formation and resulted in myocardial damage after ischemic reperfusion 25 .…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide mediated inhibition of antigen presentation from DCs to CD4+ T cells in cancer and measurement of STAT1 nitration

Markowitz

Wang

Vangundy

et al. 2017

Sci Rep

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Myeloid derived suppressor cells (MDSC) produce nitric oxide (NO) and inhibit dendritic cell (DC) immune responses in cancer. DCs present cancer cell antigens to CD4 + T cells through Jak-STAT signaltransduction. In this study, NO donors (SNAP and DETA-NONOate) inhibited DC antigen presentation. As expected, MDSC isolated from peripheral blood mononuclear cells (PBMC) from cancer patients produced high NO levels. We hypothesized that NO producing MDSC in tumor-bearing hosts would inhibit DC antigen presentation. Antigen presentation from DCs to CD4 + T cells (T cell receptor transgenic OT-II) was measured via a [ 3 H]-thymidine incorporation proliferation assay. MDSC from melanoma tumor models decreased the levels of proliferation more than pancreatic cancer derived MDSC. T cell proliferation was restored when MDSC were treated with inhibitors of inducible nitric oxide synthase (L-NAME and NCX-4016). A NO donor inhibited OT II T cell receptor recognition of OT II specific tetramers, thus serving as a direct measure of NO inhibition of antigen presentation. Our group has previously demonstrated that STAT1 nitration also mediates MDSC inhibitory effects on immune cells. Therefore, a novel liquid chromatography-tandem mass spectrometry assay demonstrated that nitration of the STAT1-Tyr701 occurs in PBMC derived from both pancreatic cancer and melanoma patients.Melanoma cells are recognized by the immune system, but the anti-tumor activity of T cells and natural killer (NK) cells is inhibited by multiple mechanisms mediated by immune suppressor cells including depletion of nutrients from the tumor microenvironment, production of reactive oxygen and nitrogen species, secretion of immune-suppressive cytokines and induction of additional inhibitory immune cells 1 . Presentation of antigens to T cells by dendritic cells (DCs) is defective in the setting of melanoma 2 . Recently, it has been shown that stimulation of DCs with type I interferons (IFN-α and β) and down-stream signal transduction via the Janus kinase-signal transducer and activator of transcription (Jak-STAT) pathway is critically important to immune surveillance and the generation of effective host T cell immune responses to cancer 3,4 . Furthermore, in dendritic cells, IFN-α signaling is responsible for up-regulation of class I and class II MHC molecules for the presentation of antigens by dendritic cells [5][6][7] . It has been demonstrated that the anti-tumor effects of IFN-α were dependent on STAT1 signal transduction in immune cells via phosphorylation of tyrosine 701 8 . Jak-STAT signaling was markedly inhibited in human peripheral blood immune cells from tumor bearing patients 9 , More recently, we

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“…In the presence of NO, cell division is inhibited in both the SN-1 and SN-2 groups. This would suggest that NO may have direct effect on the ability of the cell to form a functional mitotic or meiotic spindles (Gelaude et al, 2015), may suppress actin mediated cytokinesis or enter cell division cycle (Phung et al, 2006; Pandey et al, 2010; Pandey and Chaube, 2015). These observations suggest that NO may more specifically affect cytoskeletal proteins that are associated with cell division.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration

Fuseler

Valarmathi

2016

Front. Cell Dev. Biol.

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Nitric oxide (NO) is a small free-radical gas molecule, which is highly diffusible and can activate a wide range of downstream effectors, with rapid and widespread cellular effects. NO is a versatile signaling mediator with a plethora of cellular functions. For example, NO has been shown to regulate actin, the microfilament, dependent cellular functions, and also acts as a putative stem cell differentiation-inducing agent. In this study, using a wound-healing model of cellular migration, we have explored the effect of exogenous NO on the kinetics of movement and morphological changes in postnatal bone marrow-derived mesenchymal stem cells (MSCs). Cellular migration kinetics and morphological changes of the migrating MSCs were measured in the presence of an NO donor (S-Nitroso-N-Acetyl-D,L-Penicillamine, SNAP), especially, to track the dynamics of single-cell responses. Two experimental conditions were assessed, in which SNAP (200 μM) was applied to the MSCs. In the first experimental group (SN-1), SNAP was applied immediately following wound formation, and migration kinetics were determined for 24 h. In the second experimental group (SN-2), MSCs were pretreated for 7 days with SNAP prior to wound formation and the determination of migration kinetics. The generated displacement curves were further analyzed by non-linear regression analysis. The migration displacement of the controls and NO treated MSCs (SN-1 and SN-2) was best described by a two parameter exponential functions expressing difference constant coefficients. Additionally, changes in the fractal dimension (D) of migrating MSCs were correlated with their displacement kinetics for all the three groups. Overall, these data suggest that NO may evidently function as a stop migration signal by disordering the cytoskeletal elements required for cell movement and proliferation of MSCs.

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Nitric Oxide Donor s‐Nitroso‐n‐Acetyl Penicillamine (SNAP) Alters Meiotic Spindle Morphogenesis in Xenopus Oocytes

Cited by 8 publications

References 55 publications

From Nitric Oxide Toward S-Nitrosylation: Expanding Roles in Gametes and Embryos

From Nitric Oxide Toward S-Nitrosylation: Expanding Roles in Gametes and Embryos

Nitric oxide mediated inhibition of antigen presentation from DCs to CD4+ T cells in cancer and measurement of STAT1 nitration

Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration

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