The NF-κ B1 is a key regulator of acute but not chronic renal injury

Amy Fearn, Gerhard R. Situmorang, Christopher Fox, Fiona Oakley, Rachel Howarth, Caroline L. Wilson, Agklinta Kiosia, Michael G. Robson, Derek A. Mann, Anna Moles, Neil S. Sheerin

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)

Abstract

The NF-κ B family of transcription factors is important for many cellular functions, in particular initiation and propagation of inflammatory and immune responses. However, recent data has suggested that different subunits of the NF-κ B family can suppress the inflammatory response. NF-κ B1, from the locus nfκ b1, can inhibit transcription, acting as a brake to the recognised pro-inflammatory activity of other NF-κ B subunits. We tested the function of NF-κ B1 in an acute (nephrotoxic serum (NTS) nephritis) and a chronic (unilateral ureteric obstruction (UUO)) model of renal injury using NF-κ B1 (nfκ b1 z-/-) knockout mice. Deficiency in NF-κ B1 increased the severity of glomerular injury in NTS-induced nephritis and was associated with greater proteinuria and persistent pro-inflammatory gene expression. Induction of disease in bone marrow chimeric mice demonstrated that the absence of NF-κ B1 in either bone marrow or glomerular cells increased the severity of injury. Early after UUO (day 3) there was more severe histological injury in the nfκ b1 z-/- mice but by day 10, disease severity was equivalent in wild type and nfκ b1 z-/- mice. In conclusion, NF-κ B1 modifies acute inflammatory renal injury but does not influence chronic fibrotic injury.

Original languageEnglish
Article numbere2883
JournalCell Death and Disease
Volume8
Issue number6
DOIs
Publication statusPublished - 15 Jun 2017

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