Proteomic Modification by Nitric Oxide

Bian, Ka; Ke, Yan; Kamisaki, Yoshínori; Murad, Ferid

doi:10.1254/jphs.crj06009x

Cited by 50 publications

(29 citation statements)

References 57 publications

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“…NO generation is catalyzed by three distinct isoforms of nitric oxide synthase (NOS) (30). Two isoforms are constitutively expressed, one in endothelial cells (eNOS) and the other in the brain (nNOS) and both are calcium-dependent; the third isoform, inducible (iNOS), is regulated primarily at the transcriptional level and is calciumindependent (30). Via immunoblot analysis we documented an up-regulation of eNOS in muscle biopsies of MD patients and by confocal immunofluorescence microscopy we demonstrated its location specifically in the vessel wall.…”

Section: Discussionmentioning

confidence: 99%

Increased Protein Nitration in Mitochondrial Diseases: Evidence for Vessel Wall Involvement

Vattemi

Mechref

Marini

et al. 2011

Molecular & Cellular Proteomics

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Mitochondrial diseases (MD) are heterogeneous disorders because of impairment of respiratory chain function leading to oxidative stress. We hypothesized that in MD the vascular endothelium may be affected by increased oxidative/ nitrative stress causing a reduction of nitric oxide availability. We therefore, investigated the pathobiology of vasculature in MD patients by assaying the presence of 3-nitrotyrosine in muscle biopsies followed by the proteomic identification of proteins which undergo tyrosine nitration. We then measured the flow-mediated vasodilatation as a proof of altered nitric oxide generation/bioactivity. Here, we show that 3-nitrotyrosine staining is specifically located in the small vessels of muscle tissue and that the reaction is stronger and more evident in a significant percentage of vessels from MD patients as compared with controls. Eleven specific proteins which are nitrated under pathological conditions were identified; most of them are involved in energy metabolism and are located mainly in mitochondria. In MD patients the flow-mediated vasodilatation was reduced whereas baseline arterial diameters, blood flow velocity and endothelium-independent vasodilatation were similar to controls. The present results provide evidence that in MD the vessel wall is a target of increased oxidative/nitrative stress.

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Section: Discussionmentioning

confidence: 99%

Increased Protein Nitration in Mitochondrial Diseases: Evidence for Vessel Wall Involvement

Vattemi

Mechref

Marini

et al. 2011

Molecular & Cellular Proteomics

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“…Nonetheless, water and gases do penetrate the shell, and with this in mind the effect of NO and H 2 O 2 on encysted Artemia embryos was examined. NO and H 2 O 2 , whose activities are often integrated Bian et al, 2006;Zhang et al, 2007;Neill et al, 2008;Forman et al, 2008), were also chosen because they influence physiological and developmental processes in many organisms (Stone and Yang, 2006;Bright et al, 2006;Giorgio et al, 2007;Zhang et al, 2007;Covarrubias et al, 2008;Zhao and Shi, 2009) As demonstrated by their development in Petri plates, but not in capped tubes, the cysts examined in this study contained a subpopulation of individuals in a state of dormancy termed quiescence. These cysts failed to hatch when incubated in tubes, where for an unknown reason development was either interrupted or failed to initiate even though diapause was broken.…”

Section: Discussionmentioning

confidence: 99%

“…This report shows, for the first time to the best of our knowledge, that NO promotes postdiapause development of a crustacean embryo. NO may advance cyst development by acting as a reactive nitrogen species which drives the formation of NO-metallo linkages in haem-containing proteins (Villalobo, 2006;Forman et al, 2008), the reversible post-translational S-nitrosylation of proteins at cysteine thiol moieties (Bogdan, 2001;Ahern et al, 2002;Villalobo, 2006;Forman et al, 2008) and nitrotyrosine creation by processes either directly or indirectly mediated by H 2 O 2 (Bian et al, 2006;Villalobo, 2006;Hancock et al, 2006;Forman et al, 2008). Additionally, NO sparks guanylate cyclase activity, increasing the second messenger cyclic 3Ј,5Ј-guanosine monophosphate (cGMP), a regulator of protein kinases, phosphatases and ion channels (Aherm et al, 2002;Kim et al, 2004;Eddy, 2005;Villalobo, 2006).…”

Section: Discussionmentioning

confidence: 99%

Diapause termination and development of encystedArtemiaembryos: roles for nitric oxide and hydrogen peroxide

Robbins

Stappen

Sorgeloos

et al. 2010

Journal of Experimental Biology

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SUMMARYEncysted embryos (cysts) of the brine shrimp Artemia undergo diapause, a state of profound dormancy and enhanced stress tolerance. Upon exposure to the appropriate physical stimulus diapause terminates and embryos resume development. The regulation of diapause termination and post-diapause development is poorly understood at the molecular level, prompting this study on the capacity of hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO) to control these processes. Exposure to H 2 O 2 and NO, the latter generated by the use of three NO generators, promoted cyst development, emergence and hatching, effects nullified by catalase and the NO scavenger 2-phenyl-4,4,5,5,-tetramethylimidazoline-1-oxyl 3-oxide (PTIO). The maximal effect of NO and H 2 O 2 on cyst development was achieved by 4 h of exposure to either chemical. NO was effective at a lower concentration than H 2 O 2 but more cysts developed in response to H 2 O 2 . Promotion of development varied with incubation conditions, indicating for the first time a population of Artemia cysts potentially arrested in post-diapause and whose development was activated by either H 2 O 2 or NO. A second cyst sub-population, refractory to hatching after prolonged incubation, was considered to be in diapause, a condition broken by H 2 O 2 but not NO. These observations provide clues to the molecular mechanisms of diapause termination and development in Artemia, while enhancing the organism's value in aquaculture by affording a greater understanding of its growth and physiology.

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“…NO might signal by various mechanisms including cGMP production upon activation of NO-sensitive guanylyl cyclase (NO-GC), S-nitrosylation, tyrosine nitration and the interaction with superoxide to form peroxynitrite (Bian et al 2006), even if there is considerable evidence that NO-GC is the most important NO target during spinal nociceptive processing. Conversely, the role of NO in supraspinal pain modulation and the molecular events involved in the NO-mediated signaling pathway are poorly elucidated.…”

Section: Introductionmentioning

confidence: 99%

Reversal of NO-induced nociceptive hypersensitivity by St. John’s wort and hypericin: NF-κB, CREB and STAT1 as molecular targets

Galeotti¹,

Ghelardini²

2012

Psychopharmacology

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Rationale Hypericum perforatum, popularly called St. John's wort (SJW), is a medicinal plant mainly used as antidepressant with a favorable safety profile than standard antidepressants. Some studies have also documented other SJW bioactivities, including pain modulation. Objectives The aim of this study was to demonstrate the capability of SJW to relieve nitric oxide (NO)-induced nociceptive hypersensitivity and identify the effective component. Methods Nociceptive hypersensitivity induced by administration of the NO donors nitroglycerin (GTN) and sodium nitroprusside (SNP) was assessed by cold and hot plate tests. The cellular pathways and molecular targets involved were investigated by Western blotting. Results GTN and SNP produced a prolonged allodynia and hyperalgesia in mice. A single oral administration of low doses of an SJW dried extract or purified hypericin reversed the NO donor-induced nociceptive behavior whereas hyperforin and flavoinoids were ineffective. Investigating into the cellular pathways involved, an increased CREB and STAT1 phosphorylation, and activation of NF-κB were detected within PAG and thalamus following NO donors' administration. These cellular events were prevented by SJW or hypericin. Since hypericin showed PKC blocking properties, a role of PKC as an upstream modulator of these transcription factors was hypothesized. NO donors increased expression and phosphorylation of protein kinase C (PKC) γ and ε isoforms, molecular events prevented by SJW or hypericin. Conclusions SJW reversed NO-induced nociceptive hypersensitivity through the blockade of a supraspinal signaling pathway involving a PKC-dependent CREB, STAT1 and NF-κB activation due to presence of hypericin. These data indicate SJW/hypericin as a therapeutic perspective for pain treatment.

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Proteomic Modification by Nitric Oxide

Cited by 50 publications

References 57 publications

Increased Protein Nitration in Mitochondrial Diseases: Evidence for Vessel Wall Involvement

Increased Protein Nitration in Mitochondrial Diseases: Evidence for Vessel Wall Involvement

Diapause termination and development of encystedArtemiaembryos: roles for nitric oxide and hydrogen peroxide

Reversal of NO-induced nociceptive hypersensitivity by St. John’s wort and hypericin: NF-κB, CREB and STAT1 as molecular targets

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