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Related Experiment Video

Updated: Dec 17, 2025

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
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CD44 impacts glomerular parietal epithelial cell changes in the aged mouse kidney.

Hiroko Hamatani1,2, Diana G Eng1, Keiju Hiromura2

  • 1Division of Nephrology, University of Washington School of Medicine, Seattle, WA, USA.

Physiological Reports
|June 30, 2020
PubMed
Summary

CD44 in kidney parietal epithelial cells (PECs) drives age-related glomerular changes in mice. Deleting CD44 protected against glomerulosclerosis and preserved podocyte density in aging kidneys.

Keywords:
Bowman's capsulecorticalmTORmedullarypERKpodocyte

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Area of Science:

  • Nephrology
  • Gerontology
  • Cell Biology

Background:

  • CD44 is implicated in parietal epithelial cell (PEC) activation.
  • CD44 expression increases in PECs of aged mice, but its role is unclear.
  • Understanding CD44's function in aging kidneys is crucial for age-related kidney disease research.

Purpose of the Study:

  • To investigate the biological role of CD44 in PECs during healthy aging in mice.
  • To determine if CD44 influences age-related changes in glomerular structure and function.
  • To explore the involvement of ERK and mTOR signaling pathways.

Main Methods:

  • Comparison of young and aged CD44 knockout (CD44-/-) and wild-type (CD44+/+) mice.
  • Assessment of parietal epithelial cell density, podocyte density, and glomerulosclerosis.
  • Analysis of phosphorylated ERK 1/2 (pERK), alpha-smooth muscle actin (α-SMA), and phospho-S6 ribosomal protein (pS6RP) expression.

Main Results:

  • Aged CD44-/- mice showed reduced pERK, vimentin, and α-SMA in PECs compared to aged CD44+/+ mice.
  • Glomerular hypertrophy and glomerulosclerosis were significantly lower in aged CD44-/- mice.
  • Podocyte density was higher, and mTOR activation (pS6RP) was lower in aged CD44-/- mice.

Conclusions:

  • Increased CD44 in aged PECs contributes to glomerular changes during healthy aging.
  • CD44 appears to mediate age-related kidney alterations possibly through ERK and mTOR pathways.
  • Targeting CD44 may offer a therapeutic strategy for age-related kidney diseases.