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Related Experiment Videos

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

Aoife M Waters1, Megan Y J Wu, Tuncer Onay

  • 1Program in Developmental Biology, Research Institute, and Division of Nephrology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.

Journal of the American Society of Nephrology : JASN
|March 14, 2008
PubMed
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Constitutive Notch signaling opposes podocyte differentiation and leads to glomerulosclerosis in mice. Blocking this signaling prevents kidney damage, indicating Notch

Area of Science:

  • Nephrology
  • Developmental Biology
  • Molecular Genetics

Background:

  • Notch signaling plays a role in early podocyte development.
  • Aberrant Notch signaling may inhibit podocyte differentiation.

Purpose of the Study:

  • To investigate the impact of constitutive Notch signaling on podocyte differentiation.
  • To determine if Notch signaling is essential for mature podocyte function.

Main Methods:

  • Ectopic expression of Notch's intracellular domain (NOTCH-IC) in podocytes of transgenic mice.
  • Histologic and molecular analyses of glomerular morphology and podocyte markers.
  • Conditional inactivation of RBPJ-associated molecule (Rbpsuh) in podocytes.

Main Results:

Related Experiment Videos

  • Ectopic NOTCH-IC expression caused severe proteinuria and glomerulosclerosis in mice.
  • Mature podocyte features were lost, including effaced foot processes and downregulated Wt1, Nphs1, and Nphs2.
  • Inactivation of Rbpsuh prevented NOTCH-IC-induced kidney damage.

Conclusions:

  • Notch signaling is not essential for terminal podocyte differentiation.
  • Constitutive Notch signaling is detrimental to podocytes, causing glomerulosclerosis.
  • Targeting Notch signaling may offer therapeutic potential for kidney diseases.