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(American Journal of Pathology. 2000;156:393-398.)
© 2000 American Society for Investigative Pathology

Short Communications

Control of Apoptosis during Angiogenesis by Survivin Expression in Endothelial Cells

Daniel S. O’Connor*, Jeffrey S. Schechner*{dagger}, Colette Adida*, Mehdi Mesri*, Annette L. Rothermel*, Fengzhi Li*, Anjali K. Nath*, Jordan S. Pober*{dagger} and Dario C. Altieri*

From the Boyer Center for Molecular Medicine of the Department of Pathology*
and the Department of Dermatology,{dagger}
Yale University School of Medicine, New Haven, Connecticut

Mechanisms controlling endothelial cell survival during angiogenesis were investigated. Stimulation of quiescent endothelial cells with mitogens, including vascular endothelial growth factor and basic fibroblast growth factor, induced up to ~16-fold up-regulation of the cell cycle-regulated apoptosis inhibitor survivin. Mitogen stimulation rapidly increased survivin RNA expression in endothelial cells, which peaked after 6 to 10 hours in culture and decreased by 24 hours. Inflammatory cytokines, tumor necrosis factor {alpha}, and interleukin-1 did not induce survivin expression in endothelial cells. Formation of three-dimensional vascular tubes in vitro was associated with strong induction of survivin in endothelial cells, as compared with two-dimensional cultures. By immunohistochemistry, survivin was minimally expressed in endothelium of nonproliferating capillaries of normal skin, whereas it became massively up-regulated in newly formed blood vessels of granulation tissue in vivo. Recombinant expression of green fluorescent protein survivin in endothelial cells reduced caspase-3 activity and counteracted apoptosis induced by tumor necrosis factor {alpha}/cycloheximide. These findings identify survivin as a novel growth factor-inducible protective gene expressed by endothelial cells during angiogenesis. Therapeutic manipulation of survivin expression and function in endothelium may influence compensatory or pathological (tumor) angiogenesis.




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