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Article ; Online: Nitric oxide: a one-trick pony?

Gordge, M P

Journal of thrombosis and haemostasis : JTH

2010 Volume 8, Issue 6, Page(s) 1340–1342

MeSH term(s)	Animals ; Mice ; Nitric Oxide/physiology ; Nitric Oxide Donors/pharmacology
Chemical Substances	Nitric Oxide Donors ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2010-02-17
Publishing country	England
Document type	Comment ; Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/j.1538-7836.2010.03814.x
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Zs.MO 295: Show issues

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Article ; Online: S-nitrosothiols as selective antithrombotic agents - possible mechanisms.

Gordge, M P / Xiao, F

British journal of pharmacology

2010 Volume 159, Issue 8, Page(s) 1572–1580

Abstract: S-nitrosothiols have a number of potential clinical applications, among which their use as antithrombotic agents has been emphasized. This is largely because of their well-documented platelet inhibitory effects, which show a degree of platelet ... ...

Abstract	S-nitrosothiols have a number of potential clinical applications, among which their use as antithrombotic agents has been emphasized. This is largely because of their well-documented platelet inhibitory effects, which show a degree of platelet selectivity, although the mechanism of this remains undefined. Recent progress in understanding how nitric oxide (NO)-related signalling is delivered into cells from stable S-nitrosothiol compounds has revealed a variety of pathways, in particular denitrosation by enzymes located at the cell surface, and transport of intact S-nitrosocysteine via the amino acid transporter system-L (L-AT). Differences in the role of these pathways in platelets and vascular cells may in part explain the reported platelet-selective action. In addition, emerging evidence that S-nitrosothiols regulate key targets on the exofacial surfaces of cells involved in the thrombotic process (for example, protein disulphide isomerase, integrins and tissue factor) suggests novel antithrombotic actions, which may not even require transmembrane delivery of NO.
MeSH term(s)	Animals ; Antithrombins/pharmacology ; Hemostasis/drug effects ; Humans ; Nitric Oxide/metabolism ; S-Nitrosothiols/pharmacology ; Signal Transduction
Chemical Substances	Antithrombins ; S-Nitrosothiols ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2010-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/j.1476-5381.2010.00670.x
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Article ; Online: Inhibition of thiol isomerase activity diminishes endothelial activation of plasminogen, but not of protein C.

Smith, C L / Shah, C M / Kamaludin, N / Gordge, M P

Thrombosis research

2015 Volume 135, Issue 4, Page(s) 748–753

Abstract: Introduction: Cell surface thiol isomerase enzymes, principally protein disulphide isomerase (PDI), have emerged as important regulators of platelet function and tissue factor activation via their action on allosteric disulphide bonds. Allosteric ... ...

Abstract	Introduction: Cell surface thiol isomerase enzymes, principally protein disulphide isomerase (PDI), have emerged as important regulators of platelet function and tissue factor activation via their action on allosteric disulphide bonds. Allosteric disulphides are present in other haemostasis-related proteins, and we have therefore investigated whether thiol isomerase inhibition has any influence on two endothelial activities relevant to haemostatic regulation, namely activation of protein C and activation of plasminogen, with subsequent fibrinolysis. Materials and methods: The study was performed using the human microvascular endothelial cell line HMEC-1. Thiol isomerase gene expression was measured by RT-PCR and activation of protein C and plasminogen by cell-based assays using chromogenic substrates S2366 and S2251, respectively. Cell mediated fibrinolysis was measured by monitoring absorbance at 405 nm following fibrin clot formation on the surface of HMEC-1 monolayers. Results and conclusions: A variety of thiol isomerase enzymes, including PDI, were expressed by HMEC-1 cells and thiol reductase activity detectable on the cell surface was inhibited by both RL90 anti-PDI antibody and by the PDI inhibitor quercetin-3-rutinoside (rutin). In cell-based assays, activation of plasminogen, but not of protein C, was inhibited by RL90 antibody and, to a lesser extent, by rutin. Fibrin clot lysis occurring on a HMEC-1 monolayer was also significantly slowed by RL90 antibody and by rutin, but RL90-mediated inhibition was abolished in the presence of exogenous tissue plasminogen activator (tPA). We conclude that thiol isomerases, including PDI, are involved in fibrinolytic regulation at the endothelial surface, although not via a direct action on tPA. These findings broaden understanding of haemostatic regulation by PDI, and may aid in development of novel anti-thrombotic therapeutic strategies targeted via the fibrinolysis system.
MeSH term(s)	Fibrinolysis/physiology ; Humans ; Plasminogen/metabolism ; Protein C/metabolism ; Protein Disulfide-Isomerases/blood ; Protein Disulfide-Isomerases/genetics
Chemical Substances	Protein C ; Plasminogen (9001-91-6) ; Protein Disulfide-Isomerases (EC 5.3.4.1)
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2015.01.034
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Article: How cytotoxic is nitric oxide?

Gordge, M P

Experimental nephrology

1998 Volume 6, Issue 1, Page(s) 12–16

Abstract: Nitric oxide (NO) shows an unusual divergence of action, being utilised both as a physiological signalling molecule, and as a toxic mediator. NO-mediated cellular injury may arise by a variety of mechanisms, including disruption of mitochondrial ... ...

Abstract	Nitric oxide (NO) shows an unusual divergence of action, being utilised both as a physiological signalling molecule, and as a toxic mediator. NO-mediated cellular injury may arise by a variety of mechanisms, including disruption of mitochondrial respiration, enzyme inhibition, lipid peroxidation and genetic mutation. Toxicity is largely mediated via intermediates such as N2O3 and peroxynitrite, arising from the reaction of NO with either molecular oxygen or reactive oxygen species. In general, such reactions become significant only when high concentrations of NO are generated by the induction of nitric oxide synthase.
MeSH term(s)	Animals ; Cytotoxins ; DNA Damage ; Humans ; Lipid Peroxidation/drug effects ; Nitric Oxide/chemistry ; Nitric Oxide/pharmacology ; Oxygen Consumption/drug effects
Chemical Substances	Cytotoxins ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	1998-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1141471-6
ISSN	1421-9956 ; 1018-7782
ISSN (online)	1421-9956
ISSN	1018-7782
DOI	10.1159/000020499
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Article ; Online: Protein disulfide-isomerase mediates delivery of nitric oxide redox derivatives into platelets.

Bell, Susannah E / Shah, Chirag M / Gordge, Michael P

The Biochemical journal

2007 Volume 403, Issue 2, Page(s) 283–288

Abstract: S-nitrosothiol compounds are important mediators of NO signalling and can give rise to various redox derivatives of NO: nitrosonium cation (NO+), nitroxyl anion (NO-) and NO* radical. Several enzymes and transporters have been implicated in the ... ...

Abstract	S-nitrosothiol compounds are important mediators of NO signalling and can give rise to various redox derivatives of NO: nitrosonium cation (NO+), nitroxyl anion (NO-) and NO* radical. Several enzymes and transporters have been implicated in the intracellular delivery of NO from S-nitrosothiols. In the present study we have investigated the role of GPx (glutathione peroxidase), the L-AT (L-amino acid transporter) system and PDI (protein disulfide-isomerase) in the delivery of NO redox derivatives into human platelets. Washed human platelets were treated with inhibitors of GPx, L-AT and PDI prior to exposure to donors of NO redox derivatives (S-nitrosoglutathione, Angeli's salt and diethylamine NONOate). Rapid delivery of NO-related signalling into platelets was monitored by cGMP accumulation and DAF-FM (4-amino-5-methylamino-2'7'-difluorofluorescein) fluorescence. All NO redox donors produced both a cGMP response and DAF-FM fluorescence in target platelets. NO delivery was blocked by inhibition of PDI in a dose-dependent manner. In contrast, inhibition of GPx and L-AT had only a minimal effect on NO-related signalling.PDI activity is therefore required for the rapid delivery into platelets of NO-related signals from donors of all NO redox derivatives. GPx and the L-AT system appeared to be unimportant in rapid NO signalling by the compounds used in the present study. This does not, however, exclude a possible role during exposure of cells to other S-nitrosothiol compounds, such as S-nitrosocysteine. These results further highlight the importance of PDI in mediating the action of a wide range of NO-related signals.
MeSH term(s)	Amino Acid Transport System L/metabolism ; Arsenicals/pharmacology ; Bacitracin/pharmacology ; Biological Transport ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Cyclic GMP/metabolism ; Enzyme Inhibitors/pharmacology ; Glutathione Peroxidase/metabolism ; Guanylate Cyclase/metabolism ; Humans ; Nitric Oxide/analogs & derivatives ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Protein Disulfide-Isomerases/antagonists & inhibitors ; Protein Disulfide-Isomerases/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Soluble Guanylyl Cyclase
Chemical Substances	Amino Acid Transport System L ; Arsenicals ; Enzyme Inhibitors ; Receptors, Cytoplasmic and Nuclear ; oxophenylarsine (0HUR2WY345) ; Bacitracin (1405-87-4) ; Nitric Oxide (31C4KY9ESH) ; Glutathione Peroxidase (EC 1.11.1.9) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Protein Disulfide-Isomerases (EC 5.3.4.1) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2007-04-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BJ20061146
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Article: How Cytotoxic is Nitric Oxide?

Gordge, M.P.

Nephron Experimental Nephrology

1998 Volume 6, Issue 1, Page(s) 12–16

Institution	Institute of Urology and Nephrology, University College London, UK
Abstract	Nitric oxide (NO) shows an unusual divergence of action, being utilised both as a physiological signalling molecule, and as a toxic mediator. NO-mediated cellular injury may arise by a variety of mechanisms, including disruption of mitochondrial respiration, enzyme inhibition, lipid peroxidation and genetic mutation. Toxicity is largely mediated via intermediates such as N2O3 and peroxynitrite, arising from the reaction of NO with either molecular oxygen or reactive oxygen species. In general, such reactions become significant only when high concentrations of NO are generated by the induction of nitric oxide synthase.
Keywords	Oxidation ; Nitric oxide ; Cytotoxicity ; Peroxynitrite ; Superoxide ; Nitrosation ; Lipid peroxidation ; Mitochondria ; Enzyme inhibition
Language	English
Publishing date	1998-02-04
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Minireview
ZDB-ID	207121-6
ISSN	1660-2129 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2129 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000020499
Database	Karger publisher's database

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Article ; Online: An investigation of the protective effect of alpha+-thalassaemia against severe Plasmodium falciparum amongst children in Kumasi, Ghana.

Opoku-Okrah, C / Gordge, M / Kweku Nakua, E / Abgenyega, T / Parry, M / Robertson, C / Smith, C L

International journal of laboratory hematology

2014 Volume 36, Issue 1, Page(s) 62–70

Abstract: ... we investigate the impact of alpha+-thalassaemia genotype on P. falciparum parasitemia and prevalence of severe ... 10 years) with P. falciparum were categorised into normocytic and microcytic (mean cell volume ≤76 fL ... parasitemia (≥100 000/μL) were significantly lower (P < 0.001) in the presence of an alpha+-thalassaemia ...

Abstract	Introduction: Several factors influence the severity of Plasmodium falciparum; here, we investigate the impact of alpha+-thalassaemia genotype on P. falciparum parasitemia and prevalence of severe anaemia amongst microcytic children from Kumasi, Ghana. Methods: Seven hundred and thirty-two children (≤10 years) with P. falciparum were categorised into normocytic and microcytic (mean cell volume ≤76 fL). Microcytic individuals were genotyped for the -α(3.7) deletional thalassaemia mutation and parasite densities determined. Results: Amongst microcytic patients both parasite densities and prevalence of severe malaria parasitemia (≥100 000/μL) were significantly lower (P < 0.001) in the presence of an alpha+-thalassaemia genotype compared with non-alpha+-thalassaemia genotype. There was no evidence that alpha+-thalassaemia protected against severe anaemia. The protection conferred by alpha-thalassaemia genotype against severe P. falciparum parasitemia did not change with increasing age. Conclusion: The severity of P. falciparum parasitemia was significantly lower in both the homozygous and heterozygous alpha+-thalassaemia groups compared with microcytic individuals with non-alpha+-thalassaemia genotype. The protective effect, from severe malaria, of the alpha+-thalassaemia allele does not alter with age.
MeSH term(s)	Child ; Child, Preschool ; Erythrocyte Indices ; Erythrocytes/parasitology ; Erythrocytes/pathology ; Female ; Gene Expression ; Genotype ; Ghana ; Heterozygote ; Homozygote ; Humans ; Infant ; Infant, Newborn ; Malaria, Falciparum/blood ; Malaria, Falciparum/genetics ; Malaria, Falciparum/parasitology ; Malaria, Falciparum/pathology ; Male ; Parasitemia/blood ; Parasitemia/genetics ; Parasitemia/pathology ; Plasmodium falciparum/physiology ; Prevalence ; Protective Factors ; Severity of Illness Index ; alpha-Globins/deficiency ; alpha-Globins/genetics ; alpha-Thalassemia/blood ; alpha-Thalassemia/genetics ; alpha-Thalassemia/parasitology ; alpha-Thalassemia/pathology
Chemical Substances	alpha-Globins
Language	English
Publishing date	2014-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2268590-X
ISSN	1751-553X ; 1751-5521 ; 0141-9854
ISSN (online)	1751-553X
ISSN	1751-5521 ; 0141-9854
DOI	10.1111/ijlh.12122
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Zs.A 1499: Show issues

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Article: Interactions between cell surface protein disulphide isomerase and S-nitrosoglutathione during nitric oxide delivery.

Shah, C M / Bell, S E / Locke, I C / Chowdrey, H S / Gordge, M P

Nitric oxide : biology and chemistry

2007 Volume 16, Issue 1, Page(s) 135–142

Abstract: In this study, we investigated the role of protein disulphide isomerase (PDI) in rapid metabolism of S-nitrosoglutathione (GSNO) and S-nitrosoalbumin (albSNO) and in NO delivery from these compounds into cells. Incubation of GSNO or albSNO (1 microM) ... ...

Abstract	In this study, we investigated the role of protein disulphide isomerase (PDI) in rapid metabolism of S-nitrosoglutathione (GSNO) and S-nitrosoalbumin (albSNO) and in NO delivery from these compounds into cells. Incubation of GSNO or albSNO (1 microM) with the megakaryocyte cell line MEG-01 resulted in a cell-mediated removal of each compound which was inhibited by blocking cell surface thiols with 5,5'-dithiobis 2-nitrobenzoic acid (DTNB) (100 microM) or inhibiting PDI with bacitracin (5mM). GSNO, but not albSNO, rapidly inhibited platelet aggregation and stimulated cyclic GMP (cGMP) accumulation (used as a measure of intracellular NO entry). cGMP accumulation in response to GSNO (1 microM) was inhibited by MEG-01 treatment with bacitracin or DTNB, suggesting a role for PDI and surface thiols in NO delivery. PDI activity was present in MEG-01 conditioned medium, and was inhibited by high concentrations of GSNO (500 microM). A number of cell surface thiol-containing proteins were labelled using the impermeable thiol specific probe 3-(N-maleimido-propionyl) biocytin (MPB). Pretreatment of cells with GSNO resulted in a loss of thiol reactivity on some but not all proteins, suggesting selective cell surface thiol modification. Immunoprecipitation experiments showed that GSNO caused a concentration-dependent loss of thiol reactivity of PDI. Our data indicate that PDI is involved in both rapid metabolism of GSNO and intracellular NO delivery and that during this process PDI is itself altered by thiol modification. In contrast, the relevance of PDI-mediated albSNO metabolism to NO signalling is uncertain.
MeSH term(s)	Cell Line ; Cell Membrane/metabolism ; Cyclic GMP/metabolism ; Humans ; Immunoprecipitation ; Nitric Oxide/administration & dosage ; Protein Disulfide-Isomerases/metabolism ; S-Nitrosoglutathione/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; S-Nitrosoglutathione (57564-91-7) ; Protein Disulfide-Isomerases (EC 5.3.4.1) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2007-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2006.08.001
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Zs.A 4677: Show issues

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Article: Rapid S-nitrosothiol metabolism by platelets and megakaryocytes.

Shah, C M / Locke, I C / Chowdrey, H S / Gordge, M P

Biochemical Society transactions

2003 Volume 31, Issue Pt 6, Page(s) 1450–1452

Abstract: ... with platelets and megakaryocytes resulted in a 25-34% loss of RSNO recoverable from the supernatant (P <0.02 ...

Abstract	RSNOs (S-nitrosothiols) regulate platelet and megakaryocyte function, and may act in vivo as a nitric oxide reservoir. There is a discrepancy between the spontaneous rate of NO release from different RSNO compounds and their pharmacological effects, implying that target cells may mediate biological activity either by metabolism of RSNOs or by displaying cell surface receptors. In the present study, we sought evidence for rapid cell-mediated metabolism of RSNOs. Exposure of platelets to GSNO (S-nitrosoglutathione) for as little as 5 s inhibited thrombin-induced platelet aggregation by >95%; however, AlbSNO (S-nitrosoalbumin) was much less effective over these short time periods. Incubation of 1 microM GSNO or AlbSNO with platelets and megakaryocytes resulted in a 25-34% loss of RSNO recoverable from the supernatant (P <0.02) within 30 s. This rapid cell-mediated RSNO decay did not progress further over 5 min, and could not be accounted for by release of free NO. The gamma-glutamyl transpeptidase inhibitor acivicin (100 microM) partially decreased GSNO decay, whereas the membrane-impermeable thiol-blocking agent 5,5'-dithiobis-(2-nitrobenzoic acid) (100 microM) completely blocked cell-mediated GSNO decay and partially blocked AlbSNO decay. Our results highlight differences between high- and low-molecular-mass RSNOs with regard to their rapid metabolism/uptake and subsequent cellular responses, and indicate a critical role for extracellular thiols in RSNO metabolism by platelets and megakaryocytes.
MeSH term(s)	Blood Platelets/metabolism ; Cell Line ; Glutathione/metabolism ; Glutathione/pharmacology ; Humans ; Megakaryocytes/metabolism ; Nitroso Compounds ; S-Nitrosothiols/blood ; Serum Albumin, Bovine/metabolism ; Serum Albumin, Bovine/pharmacology
Chemical Substances	Nitroso Compounds ; S-Nitrosothiols ; S-nitrosoalbumin ; Serum Albumin, Bovine (27432CM55Q) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2003-12
Publishing country	England
Document type	Journal Article
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/bst0311450
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Article: Platelets from patients on haemodialysis show impaired responses to nitric oxide.

Gordge, M P / Neild, G H

Clinical science (London, England : 1979)

1992 Volume 83, Issue 3, Page(s) 313–318

Abstract: 1. Platelets from patients on haemodialysis showed a loss of sensitivity to nitric oxide, reflected by a reduction in the ability of nitric oxide both to inhibit thrombin-induced aggregation and to increase intraplatelet cyclic GMP levels. Responses of ... ...

Abstract	1. Platelets from patients on haemodialysis showed a loss of sensitivity to nitric oxide, reflected by a reduction in the ability of nitric oxide both to inhibit thrombin-induced aggregation and to increase intraplatelet cyclic GMP levels. Responses of platelets from patients on continuous ambulatory peritoneal dialysis were slightly, but not significantly, impaired. Platelets from both groups of uraemic patients showed normal sensitivity to the cyclic AMP-dependent inhibitor prostacyclin. 2. Reduced levels of cyclic GMP in response to nitric oxide in platelets from patients on haemodialysis were due to a defect in its generation, rather than to accelerated breakdown. 3. Basal levels of intra-platelet cyclic GMP were significantly increased in both patients on haemodialysis and patients on continuous ambulatory peritoneal dialysis. 4. The activity of nitric oxide was more stable in plasma than in buffer; its survival in plasma from patients on haemodialysis was similar to that in plasma from healthy control subjects.
MeSH term(s)	Adult ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Blood Platelets/physiology ; Cyclic GMP/metabolism ; Epoprostenol/pharmacology ; Female ; Humans ; Male ; Middle Aged ; Nitric Oxide/pharmacology ; Peritoneal Dialysis, Continuous Ambulatory/adverse effects ; Platelet Aggregation/drug effects ; Platelet Aggregation/physiology ; Renal Dialysis/adverse effects
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Epoprostenol (DCR9Z582X0) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	1992-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	760216-9
ISSN	0143-5221 ; 0144-9664
ISSN	0143-5221 ; 0144-9664
DOI	10.1042/cs0830313
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