| Literature DB >> 32197499 |
Eva Nora Bukosza1,2, Christoph Kornauth2,3, Karin Hummel4, Helga Schachner2, Nicole Huttary2, Sigurd Krieger2, Katharina Nöbauer4, André Oszwald2, Ebrahim Razzazi Fazeli4, Klaus Kratochwill5,6, Christoph Aufricht6, Gabor Szénási1, Peter Hamar1, Christoph A Gebeshuber2.
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.Entities:
Keywords: ECM; FSGS; acute phase response; complement system; fibrinogen; sclerosis
Year: 2020 PMID: 32197499 DOI: 10.3390/ijms21062095
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923