Injury Models Of The Vascular Endothelium: Apoptosis And Loss Of Thromboresistance Induced By A Viral Protein

A. Eldor*, D. Sela-Donenfeld, M. Korner, M. Pick, N. Resnick-Roguel, A. Panet

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Endothelial injury caused by viruses usually involves viral replication or transformation. We report a novel mechanism of endothelial damage by a toxic viral protein. We have isolated a new retrovirus from hemangiosarcomas which appeared among layer hens. The isolated avian hemangiosarcoma virus (AHV) is capable of inducing hemangiomas in hens in-vivo and causes a cytopathic effect (CPE) and loss of thromboresistance in cultured bovine aortic endothelial cells (BAEC). These effects do not require viral replication and can be induced by purified AHV envelope glycoprotein (gp85). AHV causes CPE in BAEC through a typical programmed cell death (apoptosis). Quiescent G0/G1-BAEC are much more sensitive to AHV induced apoptosis than actively dividing cells. These experiments demonstrate the capacity of viral proteins to affect the integrity and functionality of vascular endothelial cells.

Original languageAmerican English
Pages (from-to)37-45
Number of pages9
JournalPathophysiology of Haemostasis and Thrombosis
Volume26
DOIs
StatePublished - 1 Jan 1996

Keywords

  • Apoptosis
  • Avian hemangioma
  • Endothelial cells
  • Retrovirus
  • Thromboresistance

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