What is it about?
During the past decades, the pathogenic role of parietal epithelial cells (PECs) in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (GN) has become evident. The development of extracapillary lesions in FSGS and crescentic GN is closely associated with PEC activation. PEC activation describes the phenotypic switch from their normal quiescent state to one in which they proliferate and migrate to the glomerular tuft, leading to glomerular injury. Nonetheless, the mechanisms that drive PEC pathogenic recruitment are unknown. We demonstrated that preventing local expression of the CD9 molecules by PECs alleviates damage of the kidney's filtering units (the glomeruli) in two distinct severe diseases, Crescentic GN and FSGS. Furthermore, we demonstrated the capability of PECs to sense local changes in attracting molecules that provokes their pathogenic migration and revealed a critical facilitating role for CD9 in this process
Photo by julien Tromeur on Unsplash
Why is it important?
Taken together, Lazareth et al proved that increases in de novo CD9 expression are crucially involved in PEC activation and glomerular disease. In addition, CD9 regulates HB-EGF-EGFR and PDGFR signaling in PECs and ITGB1-mediated PEC migration. Furthermore, and more broadly, the study indicates that PECs have become crucial therapeutic targets for extracapillary diseases.
Read the Original
This page is a summary of: The tetraspanin CD9 controls migration and proliferation of parietal epithelial cells and glomerular disease progression, Nature Communications, July 2019, Springer Science + Business Media, DOI: 10.1038/s41467-019-11013-2.
You can read the full text:
The following have contributed to this page