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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Author Spotlight: Generation of Patient-Derived Podocytes from Skin Biopsies
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Podocytes are lost from glomeruli before completing apoptosis.

Kazuyoshi Yamamoto1,2, Masahiro Okabe1,2, Keiko Tanaka2

  • 1Division of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.

American Journal of Physiology. Renal Physiology
|September 1, 2022
PubMed
Summary

Podocyte apoptosis in vivo is often missed because activated podocytes detach and are lost in urine before nuclear fragmentation. Glomerular filtration aids this detachment, explaining the lack of definitive apoptotic markers in vivo.

Keywords:
apoptosiskidney diseasespodocyteproteinuria

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Area of Science:

  • Nephrology
  • Cell Biology
  • Immunology

Background:

  • Podocyte apoptosis is well-documented in vitro but poorly characterized in vivo.
  • Discrepancies in observing podocyte apoptosis in vitro versus in vivo require investigation.
  • Human CD25 (hCD25)-directed immunotoxin LMB2 is used to study podocyte cell death.

Purpose of the Study:

  • To investigate the discrepancy in podocyte apoptosis observation between in vitro and in vivo settings.
  • To elucidate the mechanism of podocyte cell death and clearance in vivo.
  • To determine the role of glomerular filtration in podocyte detachment and apoptosis.

Main Methods:

  • Cultured podocytes expressing hCD25 were treated with LMB2.
  • NEP25 mice (expressing hCD25) were treated with LMB2 to study in vivo podocyte apoptosis.
  • Unilateral ureteral obstruction and kidney organoid models were used to assess the effect of glomerular filtration.

Main Results:

  • LMB2 induced caspase-dependent apoptosis in cultured podocytes with typical apoptotic features.
  • In vivo, LMB2 eliminated hCD25-expressing podocytes, but TUNEL staining was absent, with only occasional cleaved caspase-3/lamin A positivity.
  • TUNEL-positive podocytes were found in urine, and obstructed kidneys showed increased cleaved lamin A-positive podocytes, suggesting filtration-facilitated detachment.

Conclusions:

  • Activated podocytes detach and are lost in urine before nuclear fragmentation, explaining the lack of definitive apoptosis markers in vivo.
  • Glomerular filtration actively facilitates podocyte detachment from the glomerulus.
  • This filtration-dependent detachment mechanism clarifies the infrequent observation of classical podocyte apoptosis in vivo.