Transgenic over-expression of mammalian heparanase delays prion disease onset and progression

O. Kovalchuk Ben-Zaken, I. Nissan, S. Tzaban, A. Taraboulos, E. Zcharia, S. Matzger, I. Shafat, I. Vlodavsky*, Y. Tal

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Abstract Cellular heparan sulfate (HS) has a dual role in scrapie pathogenesis; it is required for PrPSc (scrapie prion protein) formation and facilitates infection of cells, mediating cellular uptake of prions. We examined the involvement of heparanase, a mammalian endoglycosidase degrading HS, in scrapie infection. In cultured cells, heparanase treatment or over-expression resulted in a profound decrease in PrPSc. Moreover, disease onset and progression were dramatically delayed in scrapie infected transgenic mice over-expressing heparanase. Together, our results provide direct in vivo evidence for the involvement of intact HS in the pathogenesis of prion disease and the protective role of heparanase both in terms of susceptibility to infection and disease progression.

Original languageEnglish
Article number34204
Pages (from-to)698-704
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume464
Issue number3
DOIs
StatePublished - 7 Aug 2015

Bibliographical note

Publisher Copyright:
© 2015 Elsevier Inc.

Keywords

  • Heparan sulfate
  • Heparanase
  • Prion disease
  • Scrapie prion protein
  • Survival time
  • Transgenic mice

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