Pandey A, Shao H, Marks R M, Polverini P J, Dixit V M
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.
Science. 1995 Apr 28;268(5210):567-9. doi: 10.1126/science.7536959.
B61, a cytokine-inducible endothelial gene product, is the ligand for the Eck receptor protein tyrosine kinase (RPTK). Expression of a B61-immunoglobulin chimera showed that B61 could act as an angiogenic factor in vivo and a chemoattractant for endothelial cells in vitro. The Eck RPTK was activated by tumor necrosis factor-alpha (TNF-alpha) through induction of B61, and an antibody to B61 attenuated angiogenesis induced by TNF-alpha but not by basic fibroblast growth factor. This finding suggests the existence of an autocrine or paracrine loop involving activation of the Eck RPTK by its inducible ligand B61 after an inflammatory stimulus, the net effect of which would be to promote angiogenesis, a hallmark of chronic inflammation.
B61是一种细胞因子诱导的内皮基因产物，是Eck受体蛋白酪氨酸激酶（RPTK）的配体。B61-免疫球蛋白嵌合体的表达表明，B61在体内可作为血管生成因子，在体外可作为内皮细胞的趋化因子。肿瘤坏死因子-α（TNF-α）通过诱导B61激活Eck RPTK，而抗B61抗体可减弱TNF-α诱导的血管生成，但对碱性成纤维细胞生长因子诱导的血管生成无影响。这一发现提示，在炎症刺激后，存在一个自分泌或旁分泌环路，涉及Eck RPTK被其诱导性配体B61激活，其净效应是促进血管生成，这是慢性炎症的一个标志。
