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Article ; Online: Computational drug repositioning of clopidogrel as a novel therapeutic option for focal segmental glomerulosclerosis.

Gebeshuber, Christoph A / Daniel-Fischer, Lisa / Regele, Heinz / Schachner, Helga / Aufricht, Christoph / Kornauth, Christoph / Ley, Matthias / Alper, Seth L / Herzog, Rebecca / Kratochwill, Klaus / Perco, Paul

Translational research : the journal of laboratory and clinical medicine

2023 Volume 259, Page(s) 28–34

Abstract: Focal segmental glomerulosclerosis (FSGS) is a glomerular lesion often associated with nephrotic syndrome. It is also associated with a high risk of progression to end-stage kidney disease. Current treatment of FSGS is limited to systemic corticosteroids ...

Abstract	Focal segmental glomerulosclerosis (FSGS) is a glomerular lesion often associated with nephrotic syndrome. It is also associated with a high risk of progression to end-stage kidney disease. Current treatment of FSGS is limited to systemic corticosteroids or calcineurin inhibition, along with inhibitors of the renin-angiotensin-aldosterone system. FSGS is heterogeneous in etiology, and novel therapies targeting specific, dysregulated molecular pathways represent a major unmet medical need. We have generated a network-based molecular model of FSGS pathophysiology using previously established systems biology workflows to allow computational evaluation of compounds for their predicted interference with molecular processes contributing to FSGS. We identified the anti-platelet drug clopidogrel as a therapeutic option to counterbalance dysregulated FSGS pathways. This prediction of our computational screen was validated by testing clopidogrel in the adriamycin FSGS mouse model. Clopidogrel improved key FSGS outcome parameters and significantly reduced urinary albumin to creatinine ratio (P < 0.01) and weight loss (P < 0.01), and ameliorated histopathological damage (P < 0.05). Clopidogrel is used to treat several cardiovascular diseases linked to chronic kidney disease. Clopidogrel's favorable safety profile and its efficacy in the adriamycin mouse FSGS model thus recommend it as an attractive drug repositioning candidate for clinical trial in FSGS.
MeSH term(s)	Mice ; Animals ; Glomerulosclerosis, Focal Segmental/drug therapy ; Glomerulosclerosis, Focal Segmental/etiology ; Glomerulosclerosis, Focal Segmental/pathology ; Clopidogrel/pharmacology ; Clopidogrel/therapeutic use ; Drug Repositioning ; Kidney Glomerulus/pathology ; Doxorubicin/therapeutic use
Chemical Substances	Clopidogrel (A74586SNO7) ; Doxorubicin (80168379AG)
Language	English
Publishing date	2023-04-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2023.04.001
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Article ; Online: Podocyte RNA sequencing reveals Wnt- and ECM-associated genes as central in FSGS.

Bukosza, Eva Nora / Kratochwill, Klaus / Kornauth, Christoph / Schachner, Helga / Aufricht, Christoph / Gebeshuber, Christoph A

PloS one

2020 Volume 15, Issue 4, Page(s) e0231898

Abstract: Loss of podocyte differentiation can cause nephrotic-range proteinuria and Focal and Segmental Glomerulosclerosis (FSGS). As specific therapy is still lacking, FSGS frequently progresses to end-stage renal disease. The exact molecular mechanisms of FSGS ... ...

Abstract	Loss of podocyte differentiation can cause nephrotic-range proteinuria and Focal and Segmental Glomerulosclerosis (FSGS). As specific therapy is still lacking, FSGS frequently progresses to end-stage renal disease. The exact molecular mechanisms of FSGS and gene expression changes in podocytes are complex and widely unknown as marker changes have mostly been assessed on the glomerular level. To gain a better insight, we isolated podocytes of miR-193a overexpressing mice, which suffer from FSGS due to suppression of the podocyte master regulator Wt1. We characterised the podocytic gene expression changes by RNAseq and identified many novel candidate genes not linked to FSGS so far. This included strong upregulation of the receptor tyrosine kinase EphA6 and a massive dysregulation of circadian genes including the loss of the transcriptional activator Arntl. By comparison with podocyte-specific changes in other FSGS models we found a shared dysregulation of genes associated with the Wnt signaling cascade, while classical podocyte-specific genes appeared widely unaltered. An overlap with gene expression screens from human FSGS patients revealed a strong enrichment in genes associated with extra-cellular matrix (ECM) and metabolism. Our data suggest that FSGS progression might frequently depend on pathways that are often overlooked when considering podocyte homeostasis.
MeSH term(s)	Animals ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Female ; Gene Expression Regulation ; Gene Regulatory Networks ; Glomerulosclerosis, Focal Segmental/genetics ; Glomerulosclerosis, Focal Segmental/pathology ; Humans ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Podocytes/metabolism ; RNA/chemistry ; RNA/isolation & purification ; RNA/metabolism ; Receptor, EphA6/genetics ; Sequence Analysis, RNA ; WT1 Proteins/genetics
Chemical Substances	MIRN193 microRNA, mouse ; MicroRNAs ; WT1 Proteins ; RNA (63231-63-0) ; Receptor, EphA6 (EC 2.7.10.1)
Language	English
Publishing date	2020-04-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0231898
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Article ; Online: Podocyte RNA sequencing reveals Wnt- and ECM-associated genes as central in FSGS.

Eva Nora Bukosza / Klaus Kratochwill / Christoph Kornauth / Helga Schachner / Christoph Aufricht / Christoph A Gebeshuber

PLoS ONE, Vol 15, Iss 4, p e

2020 Volume 0231898

Abstract	Loss of podocyte differentiation can cause nephrotic-range proteinuria and Focal and Segmental Glomerulosclerosis (FSGS). As specific therapy is still lacking, FSGS frequently progresses to end-stage renal disease. The exact molecular mechanisms of FSGS and gene expression changes in podocytes are complex and widely unknown as marker changes have mostly been assessed on the glomerular level. To gain a better insight, we isolated podocytes of miR-193a overexpressing mice, which suffer from FSGS due to suppression of the podocyte master regulator Wt1. We characterised the podocytic gene expression changes by RNAseq and identified many novel candidate genes not linked to FSGS so far. This included strong upregulation of the receptor tyrosine kinase EphA6 and a massive dysregulation of circadian genes including the loss of the transcriptional activator Arntl. By comparison with podocyte-specific changes in other FSGS models we found a shared dysregulation of genes associated with the Wnt signaling cascade, while classical podocyte-specific genes appeared widely unaltered. An overlap with gene expression screens from human FSGS patients revealed a strong enrichment in genes associated with extra-cellular matrix (ECM) and metabolism. Our data suggest that FSGS progression might frequently depend on pathways that are often overlooked when considering podocyte homeostasis.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A systems pharmacology workflow with experimental validation to assess the potential of anakinra for treatment of focal and segmental glomerulosclerosis.

Boehm, Michael / Bukosza, Eva Nora / Huttary, Nicole / Herzog, Rebecca / Aufricht, Christoph / Kratochwill, Klaus / Gebeshuber, Christoph A

PloS one

2019 Volume 14, Issue 3, Page(s) e0214332

Abstract: Focal and Segmental Glomerulosclerosis (FSGS) is a severe glomerulopathy that frequently leads to end stage renal disease. Only a subset of patients responds to current therapies, making it important to identify alternative therapeutic options. The ... ...

Abstract	Focal and Segmental Glomerulosclerosis (FSGS) is a severe glomerulopathy that frequently leads to end stage renal disease. Only a subset of patients responds to current therapies, making it important to identify alternative therapeutic options. The interleukin (IL)-1 receptor antagonist anakinra is beneficial in several diseases with renal involvement. Here, we evaluated the potential of anakinra for FSGS treatment. Molecular process models obtained from scientific literature data were used to build FSGS pathology and anakinra mechanism of action models by exploiting information on protein interactions. These molecular models were compared by statistical interference analysis and expert based molecular signature matching. Experimental validation was performed in Adriamycin- and lipopolysaccharide (LPS)-induced nephropathy mouse models. Interference analysis (containing 225 protein coding genes and 8 molecular process segments) of the FSGS molecular pathophysiology model with the drug mechanism of action of anakinra identified a statistically significant overlap with 43 shared molecular features that were enriched in pathways relevant in FSGS, such as plasminogen activating cascade, inflammation and apoptosis. Expert adjudication of molecular signature matching, focusing on molecular process segments did not suggest a high therapeutic potential of anakinra in FSGS. In line with this, experimental validation did not result in altered proteinuria or significant changes in expression of the FSGS-relevant genes COL1A1 and NPHS1. In summary, an integrated bioinformatic and experimental workflow showed that FSGS relevant molecular processes can be significantly affected by anakinra beyond the direct drug target IL-1 receptor type 1 (IL1R1) context but might not counteract central pathophysiology processes in FSGS. Anakinra is therefore not suggested for extended preclinical trials.
MeSH term(s)	Animals ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Disease Models, Animal ; Doxorubicin/toxicity ; Drug Repositioning ; Gene Expression/drug effects ; Glomerulosclerosis, Focal Segmental/drug therapy ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/pathology ; Humans ; Interleukin 1 Receptor Antagonist Protein/pharmacology ; Interleukin 1 Receptor Antagonist Protein/therapeutic use ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Metabolic Networks and Pathways/drug effects ; Mice ; Mice, Inbred BALB C ; Podocytes/cytology ; Podocytes/drug effects ; Podocytes/metabolism
Chemical Substances	Collagen Type I ; Interleukin 1 Receptor Antagonist Protein ; Membrane Proteins ; nephrin ; Doxorubicin (80168379AG)
Language	English
Publishing date	2019-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0214332
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Article ; Online: ECM Characterization Reveals a Massive Activation of Acute Phase Response during FSGS.

Bukosza, Eva Nora / Kornauth, Christoph / Hummel, Karin / Schachner, Helga / Huttary, Nicole / Krieger, Sigurd / Nöbauer, Katharina / Oszwald, André / Razzazi Fazeli, Ebrahim / Kratochwill, Klaus / Aufricht, Christoph / Szénási, Gabor / Hamar, Peter / Gebeshuber, Christoph A

International journal of molecular sciences

2020 Volume 21, Issue 6

Abstract: The glomerular basement membrane (GBM) and extra-cellular matrix (ECM) are essential to maintain a functional interaction between the glomerular podocytes and the fenestrated endothelial cells in the formation of the slit diaphragm for the filtration of ... ...

Abstract	The glomerular basement membrane (GBM) and extra-cellular matrix (ECM) are essential to maintain a functional interaction between the glomerular podocytes and the fenestrated endothelial cells in the formation of the slit diaphragm for the filtration of blood. Dysregulation of ECM homeostasis can cause Focal segmental glomerulosclerosis (FSGS). Despite this central role, alterations in ECM composition during FSGS have not been analyzed in detail yet. Here, we characterized the ECM proteome changes in miR-193a-overexpressing mice, which suffer from FSGS due to suppression of Wilms' tumor 1 (WT1). By mass spectrometry we identified a massive activation of the acute phase response, especially the complement and fibrinogen pathways. Several protease inhibitors (ITIH1, SERPINA1, SERPINA3) were also strongly increased. Complementary analysis of RNA expression data from both miR-193a mice and human FSGS patients identified additional candidate genes also mainly involved in the acute phase response. In total, we identified more than 60 dysregulated, ECM-associated genes with potential relevance for FSGS progression. Our comprehensive analysis of a murine FSGS model and translational comparison with human data offers novel targets for FSGS therapy.
MeSH term(s)	Animals ; Complement System Proteins/metabolism ; Disease Models, Animal ; Extracellular Matrix/genetics ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Fibrinogen/metabolism ; Gene Expression Regulation ; Glomerulosclerosis, Focal Segmental/genetics ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Protease Inhibitors/metabolism
Chemical Substances	MIRN193 microRNA, mouse ; MicroRNAs ; Protease Inhibitors ; Fibrinogen (9001-32-5) ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2020-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21062095
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Article ; Online: A systems pharmacology workflow with experimental validation to assess the potential of anakinra for treatment of focal and segmental glomerulosclerosis.

Michael Boehm / Eva Nora Bukosza / Nicole Huttary / Rebecca Herzog / Christoph Aufricht / Klaus Kratochwill / Christoph A Gebeshuber

PLoS ONE, Vol 14, Iss 3, p e

2019 Volume 0214332

Abstract	Focal and Segmental Glomerulosclerosis (FSGS) is a severe glomerulopathy that frequently leads to end stage renal disease. Only a subset of patients responds to current therapies, making it important to identify alternative therapeutic options. The interleukin (IL)-1 receptor antagonist anakinra is beneficial in several diseases with renal involvement. Here, we evaluated the potential of anakinra for FSGS treatment. Molecular process models obtained from scientific literature data were used to build FSGS pathology and anakinra mechanism of action models by exploiting information on protein interactions. These molecular models were compared by statistical interference analysis and expert based molecular signature matching. Experimental validation was performed in Adriamycin- and lipopolysaccharide (LPS)-induced nephropathy mouse models. Interference analysis (containing 225 protein coding genes and 8 molecular process segments) of the FSGS molecular pathophysiology model with the drug mechanism of action of anakinra identified a statistically significant overlap with 43 shared molecular features that were enriched in pathways relevant in FSGS, such as plasminogen activating cascade, inflammation and apoptosis. Expert adjudication of molecular signature matching, focusing on molecular process segments did not suggest a high therapeutic potential of anakinra in FSGS. In line with this, experimental validation did not result in altered proteinuria or significant changes in expression of the FSGS-relevant genes COL1A1 and NPHS1. In summary, an integrated bioinformatic and experimental workflow showed that FSGS relevant molecular processes can be significantly affected by anakinra beyond the direct drug target IL-1 receptor type 1 (IL1R1) context but might not counteract central pathophysiology processes in FSGS. Anakinra is therefore not suggested for extended preclinical trials.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: ECM Characterization Reveals a Massive Activation of Acute Phase Response during FSGS

Eva Nora Bukosza / Christoph Kornauth / Karin Hummel / Helga Schachner / Nicole Huttary / Sigurd Krieger / Katharina Nöbauer / André Oszwald / Ebrahim Razzazi Fazeli / Klaus Kratochwill / Christoph Aufricht / Gabor Szénási / Peter Hamar / Christoph A. Gebeshuber

International Journal of Molecular Sciences, Vol 21, Iss 6, p

2020 Volume 2095

Abstract	The glomerular basement membrane (GBM) and extra-cellular matrix (ECM) are essential to maintain a functional interaction between the glomerular podocytes and the fenestrated endothelial cells in the formation of the slit diaphragm for the filtration of blood. Dysregulation of ECM homeostasis can cause Focal segmental glomerulosclerosis (FSGS). Despite this central role, alterations in ECM composition during FSGS have not been analyzed in detail yet. Here, we characterized the ECM proteome changes in miR-193a-overexpressing mice, which suffer from FSGS due to suppression of Wilms’ tumor 1 (WT1). By mass spectrometry we identified a massive activation of the acute phase response, especially the complement and fibrinogen pathways. Several protease inhibitors (ITIH1, SERPINA1, SERPINA3) were also strongly increased. Complementary analysis of RNA expression data from both miR-193a mice and human FSGS patients identified additional candidate genes also mainly involved in the acute phase response. In total, we identified more than 60 dysregulated, ECM-associated genes with potential relevance for FSGS progression. Our comprehensive analysis of a murine FSGS model and translational comparison with human data offers novel targets for FSGS therapy.
Keywords	fsgs ; ecm ; sclerosis ; acute phase response ; fibrinogen ; complement system ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: miR-29a suppresses tristetraprolin, which is a regulator of epithelial polarity and metastasis.

Gebeshuber, Christoph A / Zatloukal, Kurt / Martinez, Javier

EMBO reports

2009 Volume 10, Issue 4, Page(s) 400–405

Abstract: Several microRNAs (miRNAs) have recently been described as crucial regulators of epithelial-to-mesenchymal transition (EMT) and metastasis. By comparing the expression profiles of miRNAs, we found upregulation of miR-29a in mesenchymal, metastatic RasXT ... ...

Abstract	Several microRNAs (miRNAs) have recently been described as crucial regulators of epithelial-to-mesenchymal transition (EMT) and metastasis. By comparing the expression profiles of miRNAs, we found upregulation of miR-29a in mesenchymal, metastatic RasXT cells relative to epithelial EpRas cells. Overexpression of miR-29a suppressed the expression of tristetraprolin (TTP), a protein involved in the degradation of messenger RNAs with AU-rich 3'-untranslated regions, and led to EMT and metastasis in cooperation with oncogenic Ras signalling. We also observed enhanced miR-29a and reduced TTP levels in breast cancer patient samples, indicating relevance for human disease. Previously, miR-29 family members were shown to have tumour-suppressive effects in haematopoietic, cholangiocytic and lung tumours. Therefore, miRNAs can act as either oncogenes or tumour suppressors, depending on the context.
MeSH term(s)	Animals ; Blotting, Northern ; Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line ; Cell Line, Tumor ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mesoderm/metabolism ; Mesoderm/pathology ; Mice ; Mice, Nude ; MicroRNAs/genetics ; MicroRNAs/physiology ; Mutagenesis, Site-Directed ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction ; RNA, Small Interfering ; Tristetraprolin/metabolism ; Tristetraprolin/physiology
Chemical Substances	MicroRNAs ; RNA, Small Interfering ; Tristetraprolin
Language	English
Publishing date	2009-02-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/embor.2009.9
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Article ; Online: Beta-catenin/LEF-1 signalling in breast cancer--central players activated by a plethora of inputs.

Gebeshuber, Christoph A / Sladecek, Stefan / Grunert, Stefan

Cells, tissues, organs

2007 Volume 185, Issue 1-3, Page(s) 51–60

Abstract: Although the role of Wnt signalling in breast cancer is far from being fully understood, in the last years its importance has been reported frequently. Besides stimulation by canonical Wnt signalling, the downstream effectors beta-catenin and the ... ...

Abstract	Although the role of Wnt signalling in breast cancer is far from being fully understood, in the last years its importance has been reported frequently. Besides stimulation by canonical Wnt signalling, the downstream effectors beta-catenin and the transcriptional modulators of the T-cell factor/lymphoid enhancer-binding factor (TCF/LEF) family can also be activated by other inputs including the TGF-beta pathway. Wnt and TGF-beta signalling are both major signal transduction pathways, which provide important cues during development and tumor progression. However, particularly TGF-beta has a complicated influence on oncogenesis, which ranges from suppressive to promoting activity. Signalling pathways activated in parallel with TGF-beta might determine the oncogenic influence, and therefore place signals cooperating with TGF-beta into the limelight. During early development Wnt and TGF-beta signalling collaborate extensively. Here we provide an overview of the known interactions of Wnt with TGF-beta signalling in development and metastasis, particularly in breast cancer. We want to focus on the Wnt-activated transcription factor complex beta-catenin/LEF-1, its upstream activators, its downstream targets and consequences on the cellular level in response to beta-catenin/LEF-1 activation.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Humans ; Lymphoid Enhancer-Binding Factor 1/genetics ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Models, Biological ; Signal Transduction ; Smad2 Protein/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transforming Growth Factor beta/metabolism ; Wnt Proteins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	Lymphoid Enhancer-Binding Factor 1 ; Smad2 Protein ; Trans-Activators ; Transforming Growth Factor beta ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2007
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1468141-9
ISSN	1422-6421 ; 1422-6405
ISSN (online)	1422-6421
ISSN	1422-6405
DOI	10.1159/000101303
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Article ; Online: Small RNAs and their big implications: in vivo, in vitro, in silico.

Heindl, Katrin / Pezic, Dubravka / Gebeshuber, Christoph

RNA biology

2008 Volume 4, Issue 3, Page(s) 165–168

MeSH term(s)	Animals ; Computational Biology/methods ; Computational Biology/trends ; Humans ; MicroRNAs/physiology ; RNA, Small Interfering/physiology
Chemical Substances	MicroRNAs ; RNA, Small Interfering
Language	English
Publishing date	2008-02-25
Publishing country	United States
Document type	Congress
ISSN	1555-8584
ISSN (online)	1555-8584
DOI	10.4161/rna.4.3.5309
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