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Associated Projects

Associated Projects are methodologically and thematically closely linked to the SFB/TRR, but are financially independent.

DFG-Projektnummer 517717827

Heterogenität Neutrophiler Granulozyten in rheumatoider Arthritis und Systemischem Lupus

Prof. Dr. Ricardo Grieshaber-Bouyer
www.rgb-lab.de

Medizinische Klinik 3 – Rheumatologie und Immunologie
Friedrich-Alexander-Universität Erlangen-Nürnberg

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease and lupus nephritis is one of the most dangerous organ manifestations. Neutrophils are phenotypically and functionally heterogenous and play an important pathophysiologic role in SLE and rheumatoid arthritis (RA), another prototypical autoimmune disease. However, it is unclear which heterogeneity neutrophils display in RA and SLE on the single cell level and how specific effector functions in neutrophils can be targeted selectively. In this project, we will systematically dissect neutrophil heterogeneity in RA and SLE, quantify the conservation of neutrophil polarization states across humans and mice and mechanistically examine which genes influence different functional parameters in neutrophils.


DFG-Projekt LE 5009/3-1

Editing CaMKIIδ As A Therapy For Diabetic Cardiomyopathy

PD Dr. Simon Lebek

Cardiology
Universität Regensburg

The overall objective of the current project is to develop a CRISPR-Cas9 gene editing strategy to ablate the glycosylative activation site of CaMKIIδ in vivo. Several gene editing constructs will be designed and tested in vitro in HEK293 cells and extensively characterised in human iPSC-cardiomyocytes. The best editing approach will then be further optimized and applied in mice to test it as a potential therapy for diabetic cardiomyopathy in vivo. This could potentially lead to a new therapy for patients with diabetes mellitus and cardiac disease. Plus, treatment of the diabetic cardiomyopathy could also convey beneficial effects for the cardiorenal syndrome and the kidney. Specifically, our approach will include:

Objective 1: Design and optimization of the gene editing constructs in vitro

Objective 2: Functional characterization of edited human cardiomyocytes

Objective 3: Editing CaMKIIδ in vivo as a therapy for diabetic cardiomyopathy


DFG-Project SCHI 587/13-1

The role of podocytic and tubular β-catenin in proteinuric kidney disease

Prof. Dr. Mario Schiffer
Nephrology
Friedrich-Alexander-Universität Erlangen-Nürnberg

Dr. Tilman Jobst-Schwan
Nephrology
Friedrich-Alexander-Universität Erlangen-Nürnberg

Wnt/β-catenin signaling is a biologically highly conserved cellular signal transduction pathway that has important functions in embryogenesis, cell proliferation, cell differentiation and migration. It has been shown that the Wnt/β-catenin pathway is essential for regeneration and repair of tubular damage in acute kidney injury. In contrast, constant activation of Wnt/β-catenin signaling in chronic kidney disease leads to progression of the disease, so that in this case β-catenin inhibition may have protective effects. In this project, we aim to investigate how we can promote the beneficial function of β-catenin in both glomerulus and tubule, focusing particularly on proteinuric kidney disease.


DFG-PROJECT EN 453/15-1

Aufklärung der Funktion und Signalübertragung von Gpr126 bei der Entwicklung und Erkrankung der Niere

Prof. Dr. rer. nat. Dipl. Ing. Felix B. Engel
Nephropathology
Friedrich-Alexander-Universität Erlangen-Nürnberg

Chronic kidney disease represents the fastest growing pathology worldwide. Elucidating new regulators of kidney development and disease will promote the development of strategies for kidney repair. Based on our preliminary data, we conclude that
1) Gpr126 is expressed in the collecting duct,
2) in contrast to the heart, where only the NTF is required for proper development, kidney development depends on CTF and NTF,
3) Gpr126 expression is upregulated during renal disease, and
4) in renal disease Gpr126 is ectopically expressed in renal cells other than collecting duct cells.
Thus we hypothesize that Gpr126
1) contributes to the differentiation of the nephron establishing segment identity,
2) might be useful as diagnostic marker in kidney disease, and/or
3) is a promising new therapeutic target for renal diseases. Therefore, we propose to characterize the expression pattern of Gpr126 in kidney development and disease and to elucidate the role of Gpr126 function during kidney development.


  1. Deutsche Forschungsgemeinschaft (DFG)
  2. Friedrich-Alexander Universität Erlangen-Nürnberg

MISSION

"Interdisciplinary kidney research to advance understanding of disease mechanisms and develop new therapeutic concepts"

TRR374

Contact:
Dr. Michaela Kritzenberger
Email
Tel.: ++49 (0)941/943-2885
 

Molecular Medicine