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Series GSE222625 Query DataSets for GSE222625
Status Public on Jan 11, 2024
Title MyD88 deficiency in podocytes does not change the outcome in experimental glomerulonephritis.
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary Podocytes, together with glomerular endothelial cells, form the kidney filtration barrier. Loss of podocyte function leads to proteinuria and end-stage renal disease. Podocytes are damaged by various diseases. How they respond to damage-associated molecular patterns is however incompletely understood. MyD88 is the central adaptor protein downstream of Toll-like receptor (TLR) / interleukin-1 (IL-1) signaling and key to the initiation of inflammatory responses.
 
Overall design Here, we challenged WT and podocyte-specific MyD88 knockout mice (MyD88pko) with experimental glomerulonephritis (GN), nephrotoxic nephritis (NTN). Proteinuria, blood urea nitrogen (BUN) and kidney histology were used as read-outs. Podocyte ultrastructure was imaged by STED and infiltrating cells were quantified by FACS. Transcriptomic changes in podocytes of MyD88pko and WT littermate controls were analyzed under healthy and diseased conditions by bulk RNA-seq.
 
Contributor(s) Schömig T, Crispatzu G, Brinkkötter P, Brähler S
Citation(s) 38280906
Submission date Jan 11, 2023
Last update date Feb 14, 2024
Contact name Giuliano Crispatzu
Organization name University of Cologne (UoC), Germany
Department CECAD
Street address Joseph-Stelzmann-Straße 26
City Cologne
ZIP/Postal code 50931
Country Germany
 
Platforms (1)
GPL24247 Illumina NovaSeq 6000 (Mus musculus)
Samples (11)
GSM6927924 AOL_1081
GSM6927925 AOL_1082
GSM6927926 AOL_1086
Relations
BioProject PRJNA922898

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Supplementary file Size Download File type/resource
GSE222625_RAW.tar 490.7 Mb (http)(custom) TAR (of H5)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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