Gp38k, a protein synthesized by vascular smooth muscle cells, stimulates directional migration of human umbilical vein endothelial cells

Gp38k, a protein synthesized by vascular smooth muscle cells, stimulates directional migration of human umbilical vein endothelial cells
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DOI:
10.1006/excr.1999.4511
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发表时间:
1999-07-10
影响因子:
3.7
通讯作者:
Millis, AJT
Millis, AJT
中科院分区:
医学3区
文献类型:
--
作者:
Malinda, KM;Ponce, L;Millis, AJT

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Gp38k 是一种由 383 个氨基酸组成的分泌糖蛋白,由培养的血管平滑肌细胞在从增殖单层培养物过渡到非增殖多层(分化)培养物期间表达。当细胞培养物形成多细胞结节时,表达继续进行。因为这个过渡期涉及活跃的细胞迁移,我们评估了外源添加的 gp38k 对血管内皮细胞 (HUVEC) 迁移和趋化性的影响。在这里,我们证明 gp38k 作为 HUVEC 的趋化剂,刺激博伊登室中的细胞迁移,其水平与已知的内皮细胞趋化剂 bFGF 达到的水平相当。多克隆抗 gp38k 抗体的存在可以中和迁移效应。由于 gp38k 表达也与培养物形态的变化相关,因此我们还使用基质胶上生长的培养物评估了其作为 HUVEC 形态激动剂的能力。我们报告在该测定系统中 gp38k 刺激内皮细胞管生成。这些结果提供了第一个证据,表明 gp38k 可能通过刺激血管内皮细胞的迁移和重组而在血管生成中发挥作用,(C) 1999 年学术出版社。
Gp38k is a 383-amino-acid secreted glycoprotein expressed by cultured vascular smooth muscle cells during the time of transition from a proliferating monolayer culture to a nonproliferating multilayered (differentiated) culture. Expression continues as the cell culture forms multicellular nodules, Because this transition period involves active cell migration, we evaluated the effects of exogenously added gp38k on vascular endothelial cell (HUVEC) migration and chemotaxis, Here we demonstrate that gp38k acts as a chemoattractant for HUVECs and stimulates cell migration in Boyden chambers at a level comparable to that achieved with the known endothelial cell chemoattractant bFGF. The migration effect is neutralized by the presence of a polyclonal anti-gp38k antibody. Because gp38k expression is also correlated with changes in culture morphology, we also assessed its ability to act as an agonist of HUVEC morphology using cultures growing on Matrigel. We report that gp38k stimulates endothelial cell tubulogenesis in this assay system. These results provide the first evidence that gp38k may function in angiogenesis by stimulating the migration and reorganization of vascular endothelial cells, (C) 1999 Academic Press.