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Lefty antagonises TGF-beta1 induced epithelial-mesenchymal transition in tubular epithelial cells

Mythily Mariasegaram1, Greg H Tesch, Sarah Verhardt

  • 1Department of Nephrology, Monash University, Monash Medical Centre, Clayton, Vic., Australia.

Biochemical and Biophysical Research Communications
|February 23, 2010
PubMed

Insights

Lefty protein can block transforming growth factor-beta1 (TGF-beta1) from causing kidney fibrosis by preventing epithelial-mesenchymal transition (EMT). This finding suggests Lefty

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Renal Physiology

Background:

  • Transforming growth factor-beta1 (TGF-beta1) drives fibrotic diseases.
  • TGF-beta1 induces kidney fibrosis via epithelial-mesenchymal transition (EMT).
  • Lefty, a TGF supergene family member, may antagonize TGF-beta1 actions.

Purpose of the Study:

  • To investigate if Lefty can antagonize TGF-beta1-induced EMT in renal tubular epithelial cells.
  • To explore the underlying molecular mechanisms of Lefty's action.

Main Methods:

  • Stable transfection of rat tubular epithelial cells (NRK52E) with Lefty expression plasmid.
  • Exposure to TGF-beta1 to induce EMT.
  • Analysis of EMT markers (alpha-SMA, E-cadherin) and cell morphology.
  • Assessment of intracellular signaling pathways (Smad, JNK, p38).

Main Results:

  • Lefty-expressing cells (52E-Lefty) were protected from TGF-beta1-induced EMT.
  • Lefty significantly reduced TGF-beta1-induced Smad activity.
  • Lefty suppressed the secondary phase of JNK signaling, but not p38.
  • JNK inhibition also suppressed TGF-beta1-induced EMT.

Conclusions:

  • Lefty antagonizes TGF-beta1-mediated EMT in renal tubular epithelial cells.
  • Lefty demonstrates potential as an anti-fibrotic therapeutic agent for kidney fibrosis.

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