| People | Locations | Statistics |
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| Naji, M. |
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| Motta, Antonella |
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| Aletan, Dirar |
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| Mohamed, Tarek |
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| Ertürk, Emre |
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| Taccardi, Nicola |
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| Kononenko, Denys |
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| Petrov, R. H. | Madrid |
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| Alshaaer, Mazen | Brussels |
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| Bih, L. |
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| Casati, R. |
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| Muller, Hermance |
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| Kočí, Jan | Prague |
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| Šuljagić, Marija |
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| Kalteremidou, Kalliopi-Artemi | Brussels |
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| Azam, Siraj |
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| Ospanova, Alyiya |
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| Blanpain, Bart |
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| Ali, M. A. |
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| Popa, V. |
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| Rančić, M. |
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| Ollier, Nadège |
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| Azevedo, Nuno Monteiro |
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| Landes, Michael |
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| Rignanese, Gian-Marco |
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Redl, H.
in Cooperation with on an Cooperation-Score of 37%
Topics
Publications (12/12 displayed)
- 2014Ultrasound biomicroscopy (UBM) and scanning acoustic microscopy (SAM) for the assessment of hernia mesh integration: a comparison to standard histology in an experimental model.citations
- 2013Impact of mitochondria on nitrite metabolism in HL-1 cardiomyocytes.citations
- 2011Assessment of placental and bone marrow-derived stem cells for cartilage tissue engineering
- 2010Silk fibroin microparticles as carriers for delivery of human recombinant BMPs. Physical characterization and drug releasecitations
- 2010Thermoresponsive self-assembled elastin-based nanoparticles for delivery of BMPscitations
- 2010Silk fibroin microparticles as carriers for delivery of human recombinant bone morphogenetic protein-2: In vitro and in vivo bioactivitycitations
- 2008In vivo evaluation of the suitability of starch-based scaffolds for bone tissue engineering constructs using adipose derived adult stem cells and transgenic mice
- 2008Chitosan/soy-based membranes enhance wound reepithelialization in partial thickness skin wounds
- 2008Long term in vivo performance of starch-based scaffolds
- 2007Biodegradable nanomats produced by electrospinning: Expanding multifunctionality and potential for tissue engineeringcitations
- 2006Chitosan particles agglomerated scaffolds for cartilage and osteochondral tissue engineering approaches with adipose tissue derived stem cells (vol 17, pg 675, 2006)citations
- 2005Chitosan particles agglomerated scaffolds for cartilage and osteochondral tissue engineering approaches with adipose tissue derived stem cellscitations
Places of action
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article
Impact of mitochondria on nitrite metabolism in HL-1 cardiomyocytes.
Abstract
Apart from ATP synthesis mitochondria have many other functions, one being nitrite reductase activity. Nitric oxide (NO) released from nitrite has been shown to protect the heart from ischemia/reperfusion (I/R) injury in a cGMP-dependent manner. However, the exact impact of mitochondria on the release of NO from nitrite in cardiomyocytes is not completely understood. Besides mitochondria, a number of non-mitochondrial metalloproteins have been suggested to facilitate this process. The aim of this study was to investigate the impact of mitochondria on the bioactivation of nitrite in HL-1 cardiomyocytes. The levels of nitrosyl complexes of hemoglobin (NO-Hb) and cGMP levels were measured by electron spin resonance spectroscopy and enzyme immunoassay. In addition the formation of free NO was determined by confocal microscopy as well as intracellular nitrite and S-nitrosothiols by chemoluminescence analysis. NO was released from nitrite in cell culture in an oxygen-dependent manner. Application of specific inhibitors of the respiratory chain, p450, NO synthases (NOS) and xanthine oxidoreductase (XOR) showed that all four enzymatic systems are involved in the release of NO, but more than 50% of NO is released via the mitochondrial pathway. Only NO released by mitochondria activated cGMP synthesis. Cardiomyocytes co-cultured with red blood cells (RBC) competed with RBC for nitrite, but free NO was detected only in HL-1 cells suggesting that RBC are not a source of NO in this model. Apart from activation of cGMP synthesis, NO formed in HL-1 cells diffused out of the cells and formed NO-Hb complexes. In addition nitrite was converted by HL-1 cells to S-nitrosyl complexes. In HL-1 cardiomyocytes, several enzymatic systems are involved in nitrite reduction to NO but only the mitochondrial pathway of NO release activates cGMP synthesis. Our data suggest that this pathway may be a key regulator of myocardial contractility especially under hypoxic conditions.