Description
During kidney diseases, diverse tissue-specific pathways can regulate kidney injury and prognosis. In our study, we focused on STAT5, a member of the Janus Kinase/ Signal Transducer and Activator of Transcription (JAK/STAT) pathway, classically described in immune cells which has been recently described in intrinsic kidney cells. STAT5 activation is detected in both human podocytes and tubular cells in FSGS and ATI, respectively. Additionally, STAT5 deficiency in either glomerular or tubular epithelium aggravates the functional and structural alterations in a range of experimental models of glomerular or tubular disease. Using RNA sequencing, we show here that STAT5b inactivation in HEK-293 cells resulted in dysregulation of multiple metabolic pathways, including glycolysis and oxidative phosphorylation. In conclusion, activating renal epithelial STAT5 represents a new therapeutic avenue with the potential for a range of beneficial effects in kidney disease.
Overall Design
6 samples were used for this analysis : 3 HEK293 wildtype (WT) cellsand 3 HEK293 knock-out (KO)
Curator
xm_li