Angiogenesis in P- and E-selectin-deficient mice

被引：21

作者：

Hartwell, DW

Butterfield, CE

Frenette, PS

Kenyon, BM

Hynes, RO

Folkman, J

Wagner, DD

机构：

[1] Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA

[5] Childrens Hosp, Boston, MA 02115 USA

[6] MIT, Ctr Canc Res, Dept Biol, Howard Hughes Med Inst, Cambridge, MA 02139 USA

来源：

MICROCIRCULATION-LONDON | 1998年 / 5卷 / 2-3期

关键词：

angiogenesis; selectins; bFGF; TNF alpha;

D O I：

10.1038/sj.mn.7300010

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Objectives: Several observations reported earlier indicated that the selectins, in particular E-selectin, might be involved in angiogenesis; however, mice deficient in the endothelial selectins develop normally. To clarify the role of endothelial selectins in angiogenesis, we have studied experimentally induced angiogenesis in selectin-deficient mice. Methods: Hydron pellets containing either basic fibroblast growth factor or the inflammatory cytokine tumor necrosis factor alpha were implanted into the corneas of wild-type and P- and/or E-selectin-deficient mice. Results: The lengths and circumferential range of the newly formed blood vessels in the corneas of the endothelial selectin-deficient mice were similar to those of wild-type mice. Conclusion: The endothelial selectins are not essential in experimentally induced angiogenesis in vivo.

引用

页码：173 / 178

页数：6

共 23 条

[1] INTEGRIN ALPHA(V)BETA(3) ANTAGONISTS PROMOTE TUMOR-REGRESSION BY INDUCING APOPTOSIS OF ANGIOGENIC BLOOD-VESSELS [J].