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Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
07:14

Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry

Published on: October 18, 2016

Jund is a determinant of macrophage activation and is associated with glomerulonephritis susceptibility

Jacques Behmoaras1, Gurjeet Bhangal, Jennifer Smith

  • 1Physiological Genomics and Medicine Group, Medical Research Council Clinical Sciences Centre, Imperial College, Hammersmith Hospital, Du Cane Road, London, W12 0NN, UK.

Nature Genetics
|April 30, 2008
PubMed

Insights

JunD, an activator protein-1 (AP-1) transcription factor, is identified as a key factor in crescentic glomerulonephritis susceptibility. Reducing JunD levels significantly lowers macrophage activity, offering a potential therapeutic target for inflammatory kidney diseases.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • Crescentic glomerulonephritis is a major cause of kidney failure with unknown molecular underpinnings.
  • Previous studies identified seven susceptibility loci (Crgn1-Crgn7) in Wistar Kyoto (WKY) rats.

Purpose of the Study:

  • To identify the molecular basis of crescentic glomerulonephritis susceptibility.
  • To investigate the role of the Crgn2 locus in disease pathogenesis.

Main Methods:

  • Congenic, linkage, and microarray analyses were employed.
  • JunD expression was analyzed in rat and human macrophages and glomeruli.
  • JunD knockdown was performed in primary macrophages.

Main Results:

  • The activator protein-1 (AP-1) transcription factor JunD was identified as a major determinant of macrophage activity and glomerulonephritis susceptibility.
  • Introgression of the Crgn2 locus reduced crescent formation and macrophage infiltration.
  • JunD was overexpressed in susceptible WKY rat macrophages and glomeruli.
  • JunD knockdown reduced macrophage activity and cytokine secretion in both rat and human cells.

Conclusions:

  • JunD plays a critical role in macrophage activation and crescentic glomerulonephritis pathogenesis.
  • JunD function in macrophage activation is conserved between rats and humans.
  • In vivo JunD inhibition presents a potential therapeutic strategy for inflammatory and macrophage-driven kidney diseases.

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