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Structure <strong>of</strong> <strong>the</strong> Group<br />
Group Leader<br />
Pr<strong>of</strong>. Dr. Dr. Friedrich C. Luft<br />
Scientists<br />
Dr. Atakan Aydin<br />
Dr. Mira Choi<br />
Dr. Maolian Gong<br />
Pr<strong>of</strong>. Dr. Ursula Göbel<br />
PD Dr. Volkmar Gross<br />
PD Dr. Volker Homuth<br />
Dr. Martin Kann<br />
Pr<strong>of</strong>. Dr. Ralph Kettritz<br />
Carsten Lindschau<br />
Dr. Birgit Salanova<br />
Dr. Adrian Schreiber<br />
Dr. Sibylle von Vietingh<strong>of</strong>f<br />
Graduate Students<br />
Claudia Eulenberg<br />
André Gonzales<br />
Philipp Maass<br />
Gergö Molnar<br />
Nico Ruf<br />
Technical Assistants<br />
Irene Holfinger<br />
Ilona Kamer<br />
Eireen Klein<br />
Astrid Mühl<br />
Yvette Neuenfeld<br />
Petra Quass<br />
Susanne Rolle<br />
Regina Uhlmann<br />
Manager <strong>of</strong> Sponsored<br />
Programs<br />
Susannne Wissler<br />
Hypertension-induced vasculopathy<br />
Anette Fiebeler has focused on <strong>the</strong> mineralocorticoid receptor<br />
(MR) as a mediator <strong>of</strong> targent organ damage. She and<br />
her associate Gergö Molnar investigated glucocorticoidinduced<br />
MR signaling events since persons with <strong>the</strong> metabolic<br />
syndrome generally feature hypercorticoidism. The<br />
studies were derived from rodents and cell culture experiments.<br />
Rodents produce corticosterone ra<strong>the</strong>r than cortisol,<br />
which focused <strong>the</strong> groups’ attention on this metabolite. The<br />
group investigated <strong>the</strong> effects <strong>of</strong> corticosterone on early<br />
vascular MR signaling. Corticosterone initiated extracellular<br />
regulated kinase 1/2 (ERK 1/2) phosphorylation via a nongenomic<br />
effect. Corticosterone stimulated c-Jun N-terminal<br />
kinase (JNK), p38, Src, and Akt phosphorylation and potentiated<br />
Ang II-induced signaling. The team concluded that<br />
corticosterone induces rapid MR signaling in vascular<br />
smooth muscle cells that involves MEK/ERK-dependent<br />
pathways. The data suggest that glucocorticoids could contribute<br />
to vascular disease via MR signaling, independent <strong>of</strong><br />
circulating aldosterone. The findings have major <strong>the</strong>rapeutic<br />
implications.<br />
Selected Publications<br />
von Vietingh<strong>of</strong>f, S, Busjahn, A, Schonemann, C, Massenkeil, G,<br />
Otto, B, Luft, FC, Kettritz, R. (2006) Major histocompatibility<br />
complex HLA region largely explains <strong>the</strong> genetic variance exercised<br />
on neutrophil membrane proteinase 3 expression. J Am Soc<br />
Nephrol. 17, 3185-3191.<br />
von Vietingh<strong>of</strong>f, S, Tunnemann, G, Eulenberg, C, Wellner, M,<br />
Cardoso, MC, Luft, FC, Kettritz, R. (2007) NB1 mediates surface<br />
expression <strong>of</strong> <strong>the</strong> ANCA antigen proteinase 3 on human neutrophils.<br />
Blood. 109, 4487-4493.<br />
Ruf, N, Bähring, S, Galetzka, D, Pliushch, G, Luft, FC, Nürnberg,<br />
P, Haaf, T, Kelsey, G, Zechner, U. (2007) Sequence-based bioinformatic<br />
prediction and QUASEP identifying genomic imprinting<br />
<strong>of</strong> <strong>the</strong> KCNK9 potassium channel gene in mouse and human.<br />
Hum Mol Genet. 16, 2591-2599.<br />
Henke, N, Schmidt-Ullrich, R, Dechend, R, Park, JK, Qadri, F,<br />
Wellner, M, Obst, M, Gross, V, Dietz, R, Luft, FC, Scheidereit, C,<br />
Muller, DN. (2007) Vascular endo<strong>the</strong>lial cell-specific NF-κB suppression<br />
attenuates hypertension-induced renal damage. Circ<br />
Res. 101, 657-659.<br />
Bähring, S, Kann, M, Neuenfeld, Y, Gong, M, Chitayat, D, Toka,<br />
HR, Toka, O, Plessis, G, Maass, P, Rauch, A, Aydin, A, Luft, FC.<br />
(2008) The inversion region for hypertension and brachydactyly<br />
on chromosome 12p features multiple splicing and patient-specific<br />
expression <strong>of</strong> non-coding RNA. Hypertension (in press).<br />
Milestones<br />
Dominik N. Müller was awarded <strong>the</strong> Renin-Research Prize at<br />
<strong>the</strong> American Society <strong>of</strong> Hypertension Annual Meeting in<br />
Chicago, IL, USA 2007. Friedrich C. Luft was awarded <strong>the</strong><br />
Novartis Award at <strong>the</strong> American Heart Association Council<br />
For High Blood Pressure Research Annual Meeting in<br />
Tucson, AZ, USA 2007. He was <strong>the</strong> sole recipient. This award<br />
is <strong>the</strong> highest recognition in <strong>the</strong> area <strong>of</strong> hypertension-related<br />
cardiovascular research. Friedrich C. Luft will assume new<br />
duties in 2007 as director <strong>of</strong> <strong>the</strong> ECRC (see elsewhere).<br />
Cardiovascular and Metabolic Disease Research 17