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Ph Student/Naturwiss. Doktorand

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Strategies to restore mitochondrial dysfunction in acute myocardial infarction are warranted to reduce cardiomyocyte death and lethal myocardial ischemia/reperfusion (I/R) injury. This relates to the generation of toxic reactive oxygen species (ROS), deteriorated calcium signaling, permeabilization of the mitochondrial outer membrane and pertubated mitochondrial structural remodeling (fusion and fission).
Ischemic conditioning  (rIPC) applied to an organ distant from the heart, particularly before cardiac surgery-associated ischemia, provides cardioprotection. Characterization of the yet incompletely understood signaling could extend these benefits to acute coronary syndromes in general.
We have recently demonstrated that rIPC activates a hypoxic signaling in cardiomyocytes, causing posttranslational mitochondrial complex I modifications and reduced ROS. However, the impact on downstream signaling and cellular targets remains elusive. Calpains form a family of non-lysosomal cysteine proteases, which regulate cellular processes. In I/R, calpains exhibit a deleterious activity particularly affecting mitochondria. This relates to a deterioration of mitochondrial respiratory chain and a crosstalk with key signal mediators of outer membrane permeabilization and fusion/fission by cleavage of the effector Bid and affecting Bax.While calpain inhibition is generally possible, experimental studies have generated incongruent results. S-nitrosation of calpains as seen in vitro may provide a targeted modification to protect the myocardium. 

The PhD Student will persue a thesis with the questions:
(1) Can ischemic conditioning modify calpain activity in cardiomyocytes and mitochondria? For this, she/he will learn to isolate mitochondria and perform Co-IP/western blotting technique, PCR and calpain activity assays.
(2) Characterisation of the impact of calpains on mitochondrial structure. Together with our cooperation partners at the department of physics in osnabrück - this will include EPR and NMR measurements.
(3) Characterize the impact of S-nitrosation as modification on calpains in vivo.   This will include the application of biotin-switch assay, chemiluminescence, HPLC and mass spectroscopy.

The methods are to the major part established in the laboratory, further refinement and specific adaptions for the current project will be part of the thesis.


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Dr. med. Matthias Totzeck
Postdoctoral Research Fellow
Facharzt für Innere Medizin
Universitätsklinikum Düsseldorf
Klinik für Kardiologie, Pneumologie und Angiologie
Moorenstr. 5
40225 Düsseldorf
+49 170 5856490

Details der Stellenanzeige

Befristete Anstellung
Berufserfahrung nicht vorausgesetzt
Deutschland (Nordrhein-Westfalen)
40225 Düsseldorf
Healthcare & Gesundheitswesen