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CD147/Basigin Deficiency Prevents the Development of Podocyte Injury through FAK Signaling

Tomoki Yoshioka1, Tomoki Kosugi2, Tomohiro Masuda2

  • 1Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan.

The American Journal of Pathology
|April 25, 2019
PubMed

Insights

Basigin (Bsg) protein is upregulated in injured podocytes, contributing to proteinuria in kidney disease. Silencing Bsg may protect podocytes by inhibiting cell motility and signaling pathways, offering a potential therapeutic strategy.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Podocytes are crucial for kidney function and susceptible to injury, leading to proteinuric kidney diseases.
  • Urinary CD147/basigin (Bsg) levels correlate with proteinuria in focal segmental glomerulosclerosis patients.
  • The precise role of Bsg in podocyte injury remains unclear.

Purpose of the Study:

  • To elucidate the involvement of Bsg in the pathogenesis of podocyte injury.
  • To investigate the molecular mechanisms by which Bsg influences podocyte function and injury.
  • To explore Bsg silencing as a potential therapeutic strategy for proteinuric kidney diseases.

Main Methods:

  • Utilized two independent mouse models: adriamycin-induced nephropathy and L-NAME-induced endothelial dysfunction.
  • Examined Bsg expression in podocytes under normal and injured conditions.
  • Performed Bsg silencing in cultured podocytes stimulated with transforming growth factor-β (TGF-β).
  • Analyzed focal adhesion dynamics, cellular motility, and signaling pathways (β1 integrin-FAK-MMP).
  • Measured levels of vascular endothelial growth factor (VEGF) and endothelin-1 (ET-1) in cell culture supernatants.

Main Results:

  • Bsg protein is minimally expressed in healthy podocytes but induced upon injury.
  • Bsg induction in podocytes of mouse models led to podocyte effacement and proteinuria.
  • Bsg silencing in TGF-β-stimulated podocytes suppressed focal adhesion rearrangement and motility via the β1 integrin-FAK-MMP pathway.
  • Bsg silencing reduced the induction of VEGF and ET-1 in TGF-β-stimulated podocytes.
  • Bsg appears to participate in a positive feedback loop promoting podocyte motility and depolarization.

Conclusions:

  • Bsg plays a significant role in podocyte injury and the development of proteinuria.
  • Bsg silencing, by inhibiting the β1 integrin-FAK-MMP signaling pathway, offers a promising therapeutic approach.
  • Targeting Bsg may be a viable strategy to preserve podocyte integrity in proteinuric kidney diseases.

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