Gasotransmitters: Physiology and Pathophysiology

Hermann, Anton; Ситдикова, Г. Ф.; Weiger, Thomas

doi:10.1007/978-3-642-30338-8

Cited by 25 publications

(4 citation statements)

References 544 publications

(744 reference statements)

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“…Seahorse XF results are presented as means±SEM from four independent experiments (4)(5) replicates in each experiment) or as means±SD (4-5 replicates) in representative …”

Section: Statisticsmentioning

confidence: 99%

“…Recent studies conducted mainly in isolated mitochondria from various types of cells or tissues suggest that these organelles participate in the regulation of cellular activity by CO [16][17][18], but limited evidence is available in intact cells. Reiter et al [19] demonstrated CO-dependent A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 5 increase in oxygen consumption rate (OCR) in endothelial cells, which was accompanied by a disruption of mitochondrial function. In addition, Wegiel and colleagues [20] showed that CO inhibits respiration in normal cells, but CO accelerates oxidative metabolism and ROS generation and decreases glucose metabolism in cancer cells.…”

Section: Introductionmentioning

confidence: 98%

“…For a long time CO has been considered merely as a 'silent killer' due to its strong affinity to hemoglobin and high toxicity when delivered to organisms via inhalation. More recently, CO produced in low concentrations has been recognized as an important endogenous mediator involved in vascular homeostasis (for review see [3][4][5]). Being a gaseous molecule, CO can freely enter the cell and influence diverse cellular processes without the involvement of receptors or endocytosis.…”

Section: Introductionmentioning

confidence: 99%

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Carbon monoxide released by CORM-401 uncouples mitochondrial respiration and inhibits glycolysis in endothelial cells: A role for mitoBKCa channels

Kaczara

Motterlini

Rosen

et al. 2015

Biochimica et Biophysica Acta (BBA) - Bioenergetics

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Carbon monoxide (CO), a product of heme degradation by heme oxygenases, plays an important role in vascular homeostasis. Recent evidence indicates that mitochondria are among a number of molecular targets that mediate the cellular actions of CO. In the present study we characterized the effects of CO released from CORM-401 on mitochondrial respiration and glycolysis in intact human endothelial cells using electron paramagnetic resonance (EPR) oximetry and the Seahorse XF technology. We found that CORM-401 (10-100μM) induced a persistent increase in the oxygen consumption rate (OCR) that was accompanied by inhibition of glycolysis (extracellular acidification rate, ECAR) and a decrease in ATP-turnover. Furthermore, CORM-401 increased proton leak, diminished mitochondrial reserve capacity and enhanced non-mitochondrial respiration. Inactive CORM-401 (iCORM-401) neither induced mitochondrial uncoupling nor inhibited glycolysis, supporting a direct role of CO in the endothelial metabolic response induced by CORM-401. Interestingly, blockade of mitochondrial large-conductance calcium-regulated potassium ion channels (mitoBKCa) with paxilline abolished the increase in OCR promoted by CORM-401 without affecting ECAR; patch-clamp experiments confirmed that CO derived from CORM-401 activated mitoBKCa channels present in mitochondria. Conversely, stabilization of glycolysis by MG132 prevented CORM-401-mediated decrease in ECAR but did not modify the OCR response. In summary, we demonstrated in intact endothelial cells that CO induces a two-component metabolic response: uncoupling of mitochondrial respiration dependent on the activation of mitoBKCa channels and inhibition of glycolysis independent of mitoBKCa channels.

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“…Seahorse XF results are presented as means±SEM from four independent experiments (4)(5) replicates in each experiment) or as means±SD (4-5 replicates) in representative …”

Section: Statisticsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Carbon monoxide released by CORM-401 uncouples mitochondrial respiration and inhibits glycolysis in endothelial cells: A role for mitoBKCa channels

Kaczara

Motterlini

Rosen

et al. 2015

Biochimica et Biophysica Acta (BBA) - Bioenergetics

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“…Hydrogen sulfide (H 2 S) has been considered as a novel gaseous signaling molecule, similar to nitric oxide (NO) and carbon monoxide (CO) (Wagner et al 2009, Hermann et al 2012. H 2 S is produced from l-cysteine by two pyridoxal 5'-phosphate (PLP)-dependent enzymes, cystathionine β-synthase (CBS), and cystathionine γ-lyase (CSE) and PLP-independent 3-mercaptopyruvate sulfurtransferase (3MST) (Shibuya et al 2009;Singh et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Novel neuroprotective role of hydrogen sulfide in a rat model of stress brain injury

Elbassuoni

Nazmy²

2018

gpb

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Hydrogen sulfide (H2S) is a gaseous mediator recognized as important neuromodulator agent in the central nervous system. Since stress is among the most important factors involved in several pathophysiological brain processes. This study aim to investigate the effect of exogenous H2S on the possible negative effect of stress on the brain of rats and the underlying mechanisms. Rats were divided into 3 groups: control, stressed, H2S treated + stress. Brain injury markers measured were serum S100 protein and gamma enolase. Stress leads to obvious detrimental effects on the brain tissues; it produced significant increase in serum level of the above mentioned brain injury markers, and significant increase in brain levels of nitric oxide (NO), tumor necrosis factor-alpha (TNFα), and malondialdehyde (MDA) the lipid peroxidation degradative product along with significant decrease in brain glutathione level. H2S pre-treatment before stress application abolished the above detrimental effects of stress on the brain tissue since it produced significant decreases in the stressinduced expression of brain injury markers, brain TNFα, brain NO and brain MDA, and significant increases in the stress-induced reduction of brain glutathione. H2S has significant neuroprotective role in the nervous system against stress-induced significant brain injury through its antioxidant and anti-inflammatory effects.

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Homocysteine augments BK channel activity and decreases exocytosis of secretory granules in rat GH3 cells

et al. 2016

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In this study, we investigated the effects of L-homocysteine (Hcy) on maxi calcium-activated potassium (BK) channels and on exocytosis of secretory granules in GH3 rat pituitary-derived cells. A major finding of our study indicates that short-term application of Hcy increased the open probability of oxidized BK channels in inside-out recordings. Whole-cell recordings show that extracellular Hcy also augmented BK currents during long-term application. Furthermore, Hcy decreased the exocytosis of secretory granules. This decrease was partially prevented by the BK channel inhibitor paxilline and fully prevented by N-acetylcysteine, a reactive oxygen species scavenger. Taken together, our data show that elevation of cellular Hcy level induces oxidative stress, increases BK channel activity, and decreases exocytosis of secretory granules. These findings may provide insight into some of the developmental impairments and neurotoxicity associated with Hyperhomocysteinemia (HHcy), a disease arising due to abnormally elevated levels of Hcy in the plasma.

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Gasotransmitters: Physiology and Pathophysiology

Cited by 25 publications

References 544 publications

Carbon monoxide released by CORM-401 uncouples mitochondrial respiration and inhibits glycolysis in endothelial cells: A role for mitoBKCa channels

Carbon monoxide released by CORM-401 uncouples mitochondrial respiration and inhibits glycolysis in endothelial cells: A role for mitoBKCa channels

Novel neuroprotective role of hydrogen sulfide in a rat model of stress brain injury

Homocysteine augments BK channel activity and decreases exocytosis of secretory granules in rat GH3 cells

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