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Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
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CD44 deficiency increases tubular damage but reduces renal fibrosis in obstructive nephropathy

Kasper M A Rouschop1, Miguel E Sewnath, Nike Claessen

  • 1Departments of Pathology and Surgery, Academic Medical Center, Amsterdam, The Netherlands. k.m.rouschop@amc.uva.nl

Journal of the American Society of Nephrology : JASN
|February 24, 2004
PubMed

Insights

Mice lacking CD44 showed increased kidney tubular damage but reduced fibrosis after injury. CD44 (cell adhesion molecule) appears protective for tubules but promotes fibrosis by enhancing growth factor signaling.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • CD44, a glycoprotein, is upregulated in kidney injury but its role in renal damage and fibrosis is unclear.
  • CD44 mediates cell-cell and cell-matrix interactions, crucial in inflammatory and injury responses.

Purpose of the Study:

  • To investigate the role of CD44 in the pathogenesis of renal damage and fibrosis.
  • To elucidate the mechanisms by which CD44 influences kidney injury and repair.

Main Methods:

  • Utilized a mouse model of unilateral ureteral obstruction (UUO).
  • Compared CD44-deficient (CD44-/-) mice with wild-type (CD44+/+) mice.
  • Analyzed tubular damage, proliferation, apoptosis, fibrosis, macrophage influx, myofibroblast accumulation, and signaling pathways (HGF, TGF-beta1).

Main Results:

  • CD44-/- mice exhibited exacerbated tubular damage with decreased proliferation and increased apoptosis.
  • CD44-/- mice showed significantly reduced renal fibrosis post-UUO.
  • Impaired macrophage influx and myofibroblast accumulation were observed in CD44-/- mice.
  • HGF and TGF-beta1 signaling pathways were diminished in CD44-/- mice.

Conclusions:

  • CD44 plays a dual role in obstructive nephropathy: protective for tubules but promoting renal fibrosis.
  • CD44 contributes to renal fibrogenesis, partly by enhancing Hepatocyte Growth Factor (HGF) and Transforming Growth Factor-beta1 (TGF-beta1) signaling.
  • Targeting CD44 may offer therapeutic potential for mitigating renal fibrosis.

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