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2000
Volume 8, Issue 6
  • ISSN: 1573-4064
  • E-ISSN: 1875-6638

Abstract

Endoglin (CD105), a cell-surface co-receptor for transforming growth factor-beta (TGF-β) superfamily members, is over-expressed in tumor neovasculature and can be targeted with anti-endoglin antibodies, thus becoming an important tool for anti-tumoral therapy. Injury of the mouse tail induced the transient expression of endoglin, this peaking at three days after injury and disappearing six days later. An immunotoxin containing the anti-mouse endoglin rat monoclonal antibody MJ7/18 and the non-toxic ribosome-inactivating protein nigrin b (Ngb) was found to be very active in targeting mouse endoglin in the L929 fibroblast cell line (IC50 of 4 x 10-11 M). At that concentration, the immunotoxin lacked unspecific activity. Upon induction of endoglin after injury, the MJ7-Ngb immunotoxin strongly attacked and deranged the injured tail, inducing tissue damage. Such effects were dependent on the age of the animals and were evident in six-week-old mice, but not in eight-month-old mice. Our results indicate that endoglin is up-regulated in newly formed vessels upon injury and can be targeted by the MJ7-Ngb immunotoxin; thus, it could be a useful tool for tumor ablation research.

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/content/journals/mc/10.2174/157340612804075151
2012-11-01
2025-06-09
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/content/journals/mc/10.2174/157340612804075151
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  • Article Type:
    Research Article
Keyword(s): Anti-endoglin Antibody; Anti-tumor Therapy; CD105; CD105 Ablation; Endoglin; Nigrin b
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