HCKH - PI Catherine Meyer-Schwesinger - Hamburg Center for Kidney Health

Laboratory for subcellular physiology and pathophysiology

Catherine Meyer-Schwesinger

Catherine Meyer-Schwesinger

Mission Statement

“Understanding the pathophysiologic significance and signaling propensities of proteolytic systems in glomerular cells”

— Catherine Meyer-Schwesinger, MD

Team Members

Technician

Johannes Brand

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PhD Student

Sarah Frömbling

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PhD student

Lukas Heintz

PhD Student

Karen Lahme

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Post Doc

Desiree Loreth, PhD

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Post Doc

Julia Reichelt, PhD

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Post Doc

Wiebke Sachs, PhD

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PhD Student

Man Wang

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Technician

Stephanie Zielinski

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Research

Zoom

Defective protein degradation occurs in many human diseases as a primary or secondary event. The ensuing altered breakdown of macromolecules results in the generation of biomolecules, which change the intra- and intercellular signaling events, thus driving the disease at the cellular and organ level. The overarching aim of our group is to unravel the relevance and interplay of membrane bound proteases as well as of the proteasomal and lysosomal degradation systems as signaling hubs and drivers of podocyte injury, with special focus on antibody-mediated podocyte injury such as membranous nephropathy. We aim 1) at unraveling the cause of altered proteasomal function and its interplay with lysosomes in the perpetuation of disease-associated cellular processes; 2) at unraveling the sensing and communication of these alterations in disease and their effects on the intra/inter-organellar level; 3) at unraveling the contribution of membrane protein proteolysis in the development of podocyte injury.

Catherine Meyer-Schwesinger, MD

Co-director of the Institute of Cellular and Integrative Physiology

Principle Investigator

Institute of Cellular and Integrative Physiology, Center for Experimental Research

University Medical Center Hamburg-Eppendorf (UKE)
Martinistr. 52
20246 Hamburg, Germany

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CV

Current Position

since 2022	Co-director of the Institute of Cellular and Integrative Physiology, Center for Experimental Research, University Medical Center Hamburg-Eppendorf
since 2016	Principal investigator CRC 1192, Project B3

University Training

1993 - 2001

Studies of Medicine at the Albert-Ludwigs University of Freiburg Germany and at the Imperial College of London, St. Mary’s Hospital. Final grade 1,2

Academic qualifications

2012 - 2020	Habilitation (PD Dr. med.) Experimental Medicine, Center for Internal Medicine, III. Medical Clinic, University Hospital Hamburg-Eppendorf, Theme: “Podocyte Regeneration after Injury”
2001 - 2003	Post-Doctoral Fellow, University of California, San Diego, USA, Laboratory: Prof. Dr. med. Sanjay K. Nigam
1999 - 2001	MD (Dr. med.), „A new model of Age-Related Macular Degeneration"’ at the Albert-Ludwigs University Freiburg and the Harvard Medical School, Boston with Judah Folkman, USA. Grade: summa cum laude

Previous professional career

Clinical postgraduate education:

2003 - 2015

Research Associate, III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Prof. Dr. R. A. K. Stahl

Scientific postgraduate education:

2015 - 2020	Heisenberg Stipend and Professor (W3)
2013 - 2016	Principal investigator KFO 228, Project B8F

Selected awards and honors

2022 - 2020	Teacher of the Year, UKE Hamburg-Eppendorf
2020	Teacher of the Year, UKE Hamburg-Eppendorf
2019	Franz-Volhard prize of the Deutsche Gesellschaft für Nephrologie (DGfN)
2016	Dr. Martini-Preis, University of Hamburg, Germany
2001	Honors from the Albert-Ludwigs University for finishing medical studies under the top 2% in Germany
1999 - 2001	Student stipend of the Daimler-Benz Stiftung for the dissertation in Boston
1997 - 1998	DAAD study stipend for medical studies in London, Imperial College, St. Mary’s Hospital, England

Selected publications

1.	Tripartite Separation of Glomerular Cell Types and Proteomes from Reporter-Free Mice. Hatje FA, Wedekind U, Sachs W, Loreth D, Reichelt J, Demir F, Kosub C, Heintz L, Tomas NM, Huber TB, Skuza S, Sachs M, Zielinski S, Rinschen MM, Meyer-Schwesinger C. J Am Soc Nephrol. 2021 Sep;32(9):2175-2193.
2.	ADAM10-Mediated Ectodomain Shedding Is an Essential Driver of Podocyte Damage. Sachs M, Wetzel S, Reichelt J, Sachs W, Schebsdat L, Zielinski S, Seipold L, Heintz L, Müller SA, Kretz O, Lindenmeyer M, Wiech T, Huber TB, Lüllmann-Rauch R, Lichtenthaler SF, Saftig P, Meyer-Schwesinger C. J Am Soc Nephrol. 2021 Jun 1;32(6):1389-1408.
3.	Distinct Modes of Balancing Glomerular Cell Proteostasis in Mucolipidosis Type II and III Prevent Proteinuria. Sachs W, Sachs M, Krüger E, Zielinski S, Kretz O, Huber TB, Baranowsky A, Westermann LM, Voltolini Velho R, Ludwig NF, Yorgan TA, Di Lorenzo G, Kollmann K, Braulke T, Schwartz IV, Schinke T, Danyukova T, Pohl S, Meyer-Schwesinger C. J Am Soc Nephrol. 2020 Aug;31(8):1796-1814.
4.	Deubiquitinating Enzyme UCH-L1 Promotes Dendritic Cell Antigen Cross-Presentation by Favoring Recycling of MHC Class I Molecules. Reinicke AT, Raczkowski F, Mühlig M, Schmucker P, Lischke T, Reichelt J, Schneider E, Zielinski S, Sachs M, Jurack E, Tolosa E, Kurts C, Mittrücker HW, Meyer-Schwesinger C. J Immunol. 2019 Oct 1;203(7):1730-1742.
5.	Thrombospondin Type 1 Domain-Containing 7A Localizes to the Slit Diaphragm and Stabilizes Membrane Dynamics of Fully Differentiated Podocytes. Herwig J, Skuza S, Sachs W, Sachs M, Failla AV, Rune G, Meyer TN, Fester L, Meyer-Schwesinger C. J Am Soc Nephrol. 2019 May;30(5):824-839.
6.	Ubiquitin C-terminal hydrolase L1 (UCH-L1) loss causes neurodegeneration by altering protein turnover in the first postnatal weeks. Reinicke AT, Laban K, Sachs M, Kraus V, Walden M, Damme M, Sachs W, Reichelt J, Schweizer M, Janiesch PC, Duncan KE, Saftig P, Rinschen MM, Morellini F, Meyer-Schwesinger C. Proc Natl Acad Sci U S A. 2019 Apr 16;116(16):7963-7972.
7.	Ubiquitin C-Terminal Hydrolase L1 is required for regulated protein degradation through the ubiquitin proteasome system in kidney. Radón V, Czesla M, Reichelt J, Fehlert J, Hammel A, Rosendahl A, Knop JH, Wiech T, Wenzel UO, Sachs M, Reinicke AT, Stahl RAK, Meyer-Schwesinger C. Kidney Int. 2018 Jan;93(1):110-127.
8.	A Heterologous Model of Thrombospondin Type 1 Domain-Containing 7A-Associated Membranous Nephropathy. Tomas NM, Meyer-Schwesinger C, von Spiegel H, Kotb AM, Zahner G, Hoxha E, Helmchen U, Endlich N, Koch-Nolte F, Stahl RAK. J Am Soc Nephrol. 2017 Nov;28(11):3262-3277.
9.	Nanobodies that block gating of the P2X7 ion channel ameliorate inflammation. Danquah W, Meyer-Schwesinger C, Rissiek B, Pinto C, Serracant-Prat A, Amadi M, Iacenda D, Knop JH, Hammel A, Bergmann P, Schwarz N, Assunção J, Rotthier W, Haag F, Tolosa E, Bannas P, Boué-Grabot E, Magnus T, Laeremans T, Stortelers C, Koch-Nolte F. Sci Transl Med. 2016 Nov 23;8(366):366ra162.
10.	Autoantibodies against thrombospondin type 1 domain-containing 7A induce membranous nephropathy. Tomas NM, Hoxha E, Reinicke AT, Fester L, Helmchen U, Gerth J, Bachmann F, Budde K, Koch-Nolte F, Zahner G, Rune G, Lambeau G, Meyer-Schwesinger C, Stahl RA. J Clin Invest. 2016 Jul 1;126(7):2519-32.