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Updated: Feb 8, 2026

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Modified scanning electron microscopy reveals pathological crosstalk between endothelial cells and podocytes in a

Md Abdul Masum1,2, Osamu Ichii3, Yaser Hosny Ali Elewa1,4

  • 1Laboratory of Anatomy, Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.

Scientific Reports
|July 8, 2018
PubMed

Insights

This study reveals a pathological connection between endothelial cells and podocytes in membranoproliferative glomerulonephritis (MPGN) progression. Modified scanning electron microscopy (mSEM) proved useful for analyzing glomerular injury in this autoimmune kidney disease.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Membranoproliferative glomerulonephritis (MPGN) involves injury to the glomerular filtration barrier.
  • Endothelial cells and podocytes are key components of this barrier, but their interaction in MPGN pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the roles of endothelial cells and podocytes in the progression of autoimmune-mediated MPGN.
  • To evaluate the utility of modified scanning electron microscopy (mSEM) for analyzing glomerular pathology in MPGN.

Main Methods:

  • Utilized the BXSB/MpJ-Yaa mouse model of autoimmune MPGN.
  • Employed modified scanning electron microscopy (mSEM) for detailed glomerular ultrastructural analysis.
  • Assessed markers of endothelial and podocyte injury, immune cell infiltration, and renal function.

Main Results:

  • BXSB/MpJ-Yaa mice showed characteristic MPGN features including autoantibodies, albuminuria, and renal dysfunction.
  • mSEM revealed decreased glomerular endothelial fenestrations (EF) and podocyte foot process (PFP) effacement, alongside immune cell infiltration.
  • Significant reductions in endothelial (CD34, VEGF A) and podocyte (Nephrin, Podocin, Synaptopodin, WT1) markers were observed in MPGN mice.
  • Endothelial and podocyte injury indices correlated significantly with each other and with disease severity and renal dysfunction.

Conclusions:

  • Pathological crosstalk between endothelial cells and podocytes contributes to MPGN progression.
  • mSEM is a valuable tool for assessing glomerular pathological changes in MPGN.
  • Understanding these cellular interactions may offer new therapeutic targets for MPGN.

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