Semaphorin3a disrupts podocyte foot processes causing acute proteinuria

R. Tapia, F. Guan, I. Gershin, J. Teichman, G. Villegas, A. Tufro

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


Semaphorin3a was discovered as a secreted guidance protein that acts as a chemorepellent to migrating axons and endothelial cells. In the adult mouse kidney, it is expressed in podocytes and collecting tubules. Here, we show that exogenous semaphorin3a caused acute nephrotic range proteinuria associated with podocyte foot process effacement and fusion, endothelial cell damage, decreased vascular endothelial growth factor-A receptor expression, and downregulation of the slit-diaphragm proteins podocin, nephrin, and CD2-associated protein. When vascular endothelial growth factor 165 was administered at the same time as Semaphorin3a, no proteinuria or renal ultrastructural abnormalities occurred, suggesting that semaphorin3a effects may be mediated, in part, by downregulation of vascular endothelial growth factor receptor 2 signaling. Our findings indicate that a balance of semaphorin3a to vascular endothelial growth factor-A may be important for glomerular filtration barrier homeostasis.

Original languageEnglish (US)
Pages (from-to)733-740
Number of pages8
JournalKidney international
Issue number6
StatePublished - Mar 2008
Externally publishedYes


  • Podocyte effacement
  • Proteinuria
  • Semaphorin3a
  • VEGF-A
  • VEGFR2

ASJC Scopus subject areas

  • Nephrology


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