Die Rolle des Macrophage Migration Inhibitory Factor im myokardialen Ischämie-/Reperfusionsschaden : Interaktion mit der Nitrit-Signaltransduktion
Year: 2011
Type: dissertation
Abstract: In contrast to common knowledge nitrite is not an inert oxidation product of nitrogen oxide. Nitrite is reduced to NO following a physiological oxygen gradient. Therefore, nitrite is an endocrinal storage pool of NO which can be activated to influence the circulation and cellular effects. In the myocardium, nitrite reduces the ischemia/reperfusion injury and therefore it is cardioprotective. The reduction on nitrite forming NO under hypoxic conditions seems responsible for this effect. During ischemia, Myoglobin is in its deoxygenated form, which acts as a nitrite reductase. Even the cytokine Macrophage Migration Inhibitory Factor (MIF) posseses cardioprotective effects by regulating the cellular energy status after ischemia. To what extent these two factors influence each other during ischemia/reperfusion remains unclear. Using an in vitro assay, it could be shown that NO binds to the cysteines of MIF - so called S-nitrosation. This S-nitrosation is mediated by cysteine 81. Examinating infarct sizes in wildtypic mice, it became clear that nitrite is cardioprotective only if MIF is present. Reduction of reactive oxygen species and the decrease of oxidative protein damage seems to be responsible for the cardioprotective effects. This dissertation provides an first insight into the mechanism of the properties of nitrite during myocardial ischemia/reperfusion. Elucidating the nitrite properties can be helpful finding a treatment for the reperfusion injury after myocardial infarction.
Source: RWTH Publications (RWTH Aachen)
Authors: Julia Sobierajski, Tienush Rassaf
Language: German
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2337005593