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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Differential expression of transforming growth factor-beta isoforms and receptors in experimental membranous

S J Shankland1, J Pippin, R H Pichler

  • 1Division of Nephrology, University of Washington, Seattle, USA.

Kidney International
|July 1, 1996
PubMed

Insights

Complement-mediated injury in membranous nephropathy (MN) upregulates TGF-beta 2 and TGF-beta 3 in glomerular epithelial cells (GEC). This study highlights the role of these TGF-beta isoforms in GEC response to injury.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Biology

Background:

  • Membranous nephropathy (MN) involves matrix overproduction by glomerular epithelial cells (GEC), leading to glomerular basement membrane thickening.
  • The specific molecular mechanisms driving GEC matrix production in MN require further elucidation.

Purpose of the Study:

  • To investigate the role of transforming growth factor-beta (TGF-beta) isoforms and their receptors in experimental membranous nephropathy (MN).
  • To determine if complement-mediated injury influences TGF-beta signaling in glomerular epithelial cells (GEC).

Main Methods:

  • Studied passive Heymann nephritis (PHN) in rats at 5, 10, and 30 days.
  • Assessed immunostaining and glomerular mRNA levels for TGF-beta isoforms (1, 2, 3) and their receptors (T beta RI, T beta RII).
  • Evaluated TGF-beta 2 bioactivity and the effect of complement depletion.

Main Results:

  • PHN rats showed increased GEC immunostaining for TGF-beta 2 at all time points and TGF-beta 3 at day 10.
  • Glomerular mRNA for TGF-beta 2 and -beta 3 increased by day 5, coinciding with increased urine protein.
  • Increased expression and mRNA levels of TGF-beta 2, TGF-beta 3, T beta RI, and T beta RII were prevented by complement depletion.

Conclusions:

  • Complement-mediated GEC injury in vivo upregulates TGF-beta 2 and -beta 3 isoforms and their receptors.
  • Increased TGF-beta 2 bioactivity suggests a functional role in experimental MN.
  • TGF-beta 2 and -beta 3, rather than TGF-beta 1, appear critical in GEC-specific responses to injury in MN.

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