Takakura Nobuyuki, Huang Xu-Ling, Naruse Takeshi, Hamaguchi Isao, Dumont Daniel J, Yancopoulos George D, Suda Toshio
Department of Cell Differentiation, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Japan.
Immunity. 1998 Nov;9(5):677-86. doi: 10.1016/s1074-7613(00)80665-2.
We have investigated the function of TIE2/TEK receptor tyrosine kinase in the development of definitive hematopoiesis. In the vitelline artery at 9.5 days postcoitum (d.p.c.), TIE2+ hematopoietic cells aggregated and adhered to TIE2+ endothelial cells. Soluble TIE2-Fc chimeric protein inhibited the development of hematopoiesis and angiogenesis in the para-aortic splanchnopleural mesoderm (P-Sp) explant culture, and TIE2-deficient mice showed severely impaired definitive hematopoiesis. An in vitro study revealed that Angiopoietin-1 but not Angiopoietin-2 promoted the adhesion to fibronectin (FN) through integrins in TIE2-transfected cells and primary TIE2+ cells sorted from 9.5 d.p.c. P-Sp. Adhesion of TIE2+ cells induced by Angiopoietin-1 enhanced the proliferation of hematopoietic progenitor cells.
我们研究了TIE2/TEK受体酪氨酸激酶在确定性造血发育中的功能。在妊娠9.5天（d.p.c.）的卵黄动脉中，TIE2+造血细胞聚集并黏附于TIE2+内皮细胞。可溶性TIE2-Fc嵌合蛋白抑制了主动脉旁脏壁中胚层（P-Sp）外植体培养中造血和血管生成的发育，且TIE2缺陷小鼠的确定性造血严重受损。一项体外研究表明，血管生成素-1而非血管生成素-2通过整合素促进TIE2转染细胞以及从9.5 d.p.c.的P-Sp中分选的原代TIE2+细胞与纤连蛋白（FN）的黏附。血管生成素-1诱导的TIE2+细胞黏附增强了造血祖细胞的增殖。
