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Related Experiment Videos

Regulated expression of complement factor B in the human kidney

T R Welch1, L S Beischel, M Frenzke

  • 1Division of Nephrology, Children's Hospital Research Foundation, Cincinnati, Ohio, USA.

Kidney International
|August 1, 1996
PubMed
Summary
This summary is machine-generated.

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Human kidneys show local production of complement factors C3 and factor B in proximal tubules. This suggests these proteins may drive interstitial inflammation in chronic kidney disease.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Regulated expression of complement component 3 (C3) in human proximal tubular epithelial cells is known.
  • The role of local alternative pathway complement activation in chronic kidney disease pathogenesis is under investigation.

Purpose of the Study:

  • To test the hypothesis that local alternative pathway complement activation contributes to tubulointerstitial inflammation in chronic renal disease.
  • To examine factor B gene expression in human kidneys.

Main Methods:

  • Generated 35S riboprobes from human factor B cDNA.
  • Utilized in situ hybridization to detect factor B gene expression in kidney tissues.

Main Results:

  • Proximal tubular factor B messenger RNA (mRNA) was detected in 17 human kidneys with nephropathies.

Related Experiment Videos

  • Factor B expression intensity correlated with interstitial inflammation.
  • Factor B mRNA was not found in glomeruli or infiltrating inflammatory cells.
  • Normal kidney tissues showed absent or minimal factor B expression.

    • Conclusions:

    • Human proximal renal tubular epithelium expresses genes for both C3 and factor B, key components of the alternative pathway convertase.
    • Locally produced C3 and factor B may mediate interstitial inflammation common to progressive nephritides.