Abstract:
:The mechanisms driving the development of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly understood. A key question is how parietal epithelial cells (PECs) invade glomerular capillaries, thereby promoting injury and kidney failure. Here we show that expression of the tetraspanin CD9 increases markedly in PECs in mouse models of CGN and FSGS, and in kidneys from individuals diagnosed with these diseases. Cd9 gene targeting in PECs prevents glomerular damage in CGN and FSGS mouse models. Mechanistically, CD9 deficiency prevents the oriented migration of PECs into the glomerular tuft and their acquisition of CD44 and β1 integrin expression. These findings highlight a critical role for de novo expression of CD9 as a common pathogenic switch driving the PEC phenotype in CGN and FSGS, while offering a potential therapeutic avenue to treat these conditions.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Lazareth H,Henique C,Lenoir O,Puelles VG,Flamant M,Bollée G,Fligny C,Camus M,Guyonnet L,Millien C,Gaillard F,Chipont A,Robin B,Fabrega S,Dhaun N,Camerer E,Kretz O,Grahammer F,Braun F,Huber TB,Nochy D,Mandet C,doi
10.1038/s41467-019-11013-2subject
Has Abstractpub_date
2019-07-24 00:00:00pages
3303issue
1issn
2041-1723pii
10.1038/s41467-019-11013-2journal_volume
10pub_type
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