Nitric oxide, cell signaling and cell death

Blaise, Gilbert; Gauvin, Dominique; Gangal, Marius; Authier, Simon

doi:10.1016/j.tox.2004.11.032

Cited by 224 publications

(144 citation statements)

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“…[7] The pronounced effect of NAMI-A on angiogenesis was confirmed in the chick allantoic membrane and in the rabbit eye cornea model. [8,9] It should be also noted that NO, which is produced by a number of nitric oxide synthase (NOS) enzymes from larginine in the body, [10] plays a major role as a signaling molecule in biological signal transducing systems, for example, in blood pressure regulation, [11,12] neurotransmission, [13,14] inflammatory response, [15,16] as well as necrosis [17] and apoptosis. [18,19] Nitric oxide is therefore essential in biological systems, but both its excess as well as deficiency leads to pathologies.…”

Section: Introductionmentioning

confidence: 99%

On the Electronic Structure ofmer,trans‐[RuCl₃(1H‐indazole)₂(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

et al. 2013

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The study reported herein focused on the electronic structure of the {Ru(NO)} 6 fragment and characterization of the oxidation state of ruthenium in mer,trans- [RuCl 3 (Hind) (3) were experimentally and theoretically investigated as reference compounds. A complete active space SCF calculation was performed to estimate the extent of antiferromagnetic spin-spin coupling in 1. We found that the closed-shell structure {Ru III (NO) 0 } 6 fits better to the physical/ spectroscopic properties of 1, although {Ru II (NO) + } 6 is formally still suitable for describing the oxidation state of Ru in this entity.

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Section: Introductionmentioning

confidence: 99%

On the Electronic Structure ofmer,trans‐[RuCl₃(1H‐indazole)₂(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

et al. 2013

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“…Within the nervous system, NO normally functions as an endogenous neurotransmitter [23] but exposure to levels beyond those necessary for physiological activity may be highly toxic in neuronal cells [24]. Low doses of NO can also be cytoprotective [21], mainly through a cGMP-mediated signaling mechanism [21,[25][26][27] or through caspase inhibition [28].…”

Section: Introductionmentioning

confidence: 99%

Nerve Growth Factor Potentiates p53 DNA Binding but Inhibits Nitric Oxide-Induced Apoptosis in Neuronal PC12 Cells

Brynczka

Merrick

2007

Neurochem Res

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NGF is recognized for its role in neuronal differentiation and maintenance. Differentiation of PC12 cells by NGF involves p53, a transcription factor that controls growth arrest and apoptosis. We investigated NGF influence over p53 activity during NO-induced apoptosis by sodium nitroprusside in differentiated and mitotic PC12 cells. NGF-differentiation produced increased p53 levels, nuclear localization and sequence-specific DNA binding. Apoptosis in mitotic cells also produced these events but the accompanying activation of caspases 1-10 and mitochondrial depolarization were inhibited during NGF differentiation and could be reversed in p53-silenced cells. Transcriptional regulation of PUMA and survivin expression were not inhibited by NGF, although NO-induced mitochondrial depolarization was dependent upon de novo gene transcription and only occurred in mitotic cells. We conclude that NGF mediates prosurvival signaling by increasing factors such as Bcl-2 and p21 Waf1/Cip1 without altering p53 transcriptional activity and prevents mitochondrial depolarization and caspase activation to inhibit apoptosis.

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“…The diatomic messenger NO and sGC play a critical role in several physiological processes: regulation of vascular blood pressure and cardiovascular diseases (3), lung airway relaxation and pulmonary pathologies (4), immune response and inflammatory disorders (5), and tumor progression and apoptosis (6). Thus, sGC is a pharmacological target of very high interest, and several activators have been developed (7,8), leading to the approval of riociguat for the treatment of pulmonary hypertension (9,10).…”

mentioning

confidence: 99%

Motion of proximal histidine and structural allosteric transition in soluble guanylate cyclase

Yoo

Lamarre

Martin

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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We investigated the changes of heme coordination in purified soluble guanylate cyclase (sGC) by time-resolved spectroscopy in a time range encompassing 11 orders of magnitude (from 1 ps to 0.2 s). After dissociation, NO either recombines geminately to the 4-coordinate (4c) heme (τ G1 = 7.5 ps; 97 ± 1% of the population) or exits the heme pocket (3 ± 1%). The proximal His rebinds to the 4c heme with a 70-ps time constant. Then, NO is distributed in two approximately equal populations (1.5%). One geminately rebinds to the 5c heme (τ G2 = 6.5 ns), whereas the other diffuses out to the solution, from where it rebinds bimolecularly (τ = 50 μs with [NO] = 200 μM) forming a 6c heme with a diffusion-limited rate constant of 2 × 10 8 M −1 ·s −1 . In both cases, the rebinding of NO induces the cleavage of the Fe-His bond that can be observed as an individual reaction step. Saliently, the time constant of bond cleavage differs depending on whether NO binds geminately or from solution (τ 5C1 = 0.66 μs and τ 5C2 = 10 ms, respectively). Because the same event occurs with rates separated by four orders of magnitude, this measurement implies that sGC is in different structural states in both cases, having different strain exerted on the Fe-His bond. We show here that this structural allosteric transition takes place in the range 1-50 μs. In this context, the detection of NO binding to the proximal side of sGC heme is discussed.soluble guanylate cyclase | nitric oxide | time-resolved absorption spectroscopy | allostery | protein activation T he soluble guanylate cyclase (sGC), localized in many different cell types, is the receptor of the endogenous messenger nitric oxide (NO) and catalyzes the formation of cGMP from GTP upon activation triggered by NO binding (1, 2). The diatomic messenger NO and sGC play a critical role in several physiological processes: regulation of vascular blood pressure and cardiovascular diseases (3), lung airway relaxation and pulmonary pathologies (4), immune response and inflammatory disorders (5), and tumor progression and apoptosis (6). Thus, sGC is a pharmacological target of very high interest, and several activators have been developed (7,8), leading to the approval of riociguat for the treatment of pulmonary hypertension (9, 10). Because of its pharmacological interest, the mechanisms of activation, deactivation, and regulation of sGC must be deciphered at the molecular level. Despite numerous efforts, the 3D crystal structure of heterodimeric sGC remains unknown, but the heme domain of the sGC β1-subunit [called heme NO/oxygen-binding (H-NOX)] was modeled from the heme domain of bacterial NO sensors (11,12) and the sGC catalytic α1-subunit was modeled from the catalytic α1-subunit of adenylate cyclase (13). Recently, the entire quaternary structure of sGC was reconstructed by inserting individual protein domains into the density envelope of entire single-sGC molecules observed by EM (14), revealing a high flexibility of the sGC dimer. Subsequently, the structural perturbations induced by NO bi...

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Nitric oxide, cell signaling and cell death

Cited by 224 publications

References 133 publications

On the Electronic Structure ofmer,trans‐[RuCl₃(1H‐indazole)₂(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

On the Electronic Structure ofmer,trans‐[RuCl₃(1H‐indazole)₂(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

Nerve Growth Factor Potentiates p53 DNA Binding but Inhibits Nitric Oxide-Induced Apoptosis in Neuronal PC12 Cells

Motion of proximal histidine and structural allosteric transition in soluble guanylate cyclase

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Nitric oxide, cell signaling and cell death

Cited by 224 publications

References 133 publications

On the Electronic Structure ofmer,trans‐[RuCl3(1H‐indazole)2(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

On the Electronic Structure ofmer,trans‐[RuCl3(1H‐indazole)2(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

Nerve Growth Factor Potentiates p53 DNA Binding but Inhibits Nitric Oxide-Induced Apoptosis in Neuronal PC12 Cells

Motion of proximal histidine and structural allosteric transition in soluble guanylate cyclase

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On the Electronic Structure ofmer,trans‐[RuCl₃(1H‐indazole)₂(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study

On the Electronic Structure ofmer,trans‐[RuCl₃(1H‐indazole)₂(NO)], a Hypothetical Metabolite of the Antitumor Drug Candidate KP1019: An Experimental and DFT Study