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作 者:徐启河[1] 陈香美[1] 傅博[1] 叶一舟[1] 于力方[1]
机构地区:[1]解放军总医院
出 处:《解放军医学杂志》1999年第3期160-164,共5页Medical Journal of Chinese People's Liberation Army
基 金:国家自然科学基金;"九.五"军队医药卫生科研基金
摘 要:观察了体外培养的人类肾小球内皮细胞(GEC)在纤维蛋白凝胶上的生长状态,以及在GEC表面覆盖纤维蛋白凝胶对GEC表型的影响,并进行了干预试验。结果发现,GEC在纤维蛋白凝胶包被的细胞培养板上培养可以自发地形成典型的血管样结构。αvβ3整合素单抗23C6可以显著促进纤维蛋白介导的血管样结构的形成,而精氨酰-甘氨酰-天门冬氨酰-丝氨酸(RGDS)四肽、放线菌酮、放线菌素D对血管样结构的形成具有抑制作用(P<0.001)。在融合态GEC细胞单层表面原位形成des-AA-纤维蛋白或des-AABB-纤维蛋白凝胶均可引起GEC单层结构破坏,肝素、放线菌酮、放线菌素D、非免疫小鼠IgG以及精氨酰-甘氨酰-甘氨酰-丝氨酸(RGGS)四肽不能阻断纤维蛋白诱导的GEC单层结构破坏,而23C6、RGDS四肽可以完全阻断上述改变。说明αvβ3整合素-RGDS位点相互作用介导了纤维蛋白所致GEC单层结构破坏和血管样结构形成,RGDS四肽防治纤维蛋白所诱发的GEC表型变化可能具有潜在的价值。In vitro studies were carried out to observe the growing status of human glomerular endothelial cells (GECs) stimulated by covering and underlying fibrin gels in the presence or absence of antiv3 integrin monoclonal antibody 23C6,synthetic RGDS peptide, heparin, cycloheximide, and actinomycin D, respectively. Results: GECs developed capillary tube structure on fibrin gel, which was promoted by 23C6, but inhibited by RGDS peptide, cycloheximide, and actinomycin D (P<0.001). Similar and specific disorganization of GEC monolayers was induced by covering them with desAAfibrin and desAABBfibrin , and this phenomenon was prevented by antiv3 integrin 23C6 and synthetic RGDS peptide , while nonimmune mouse IgG, synthetic RGGS peptide, cycloheximide, and actinomycin D had no similar effects. It is concluded that GECs cultured on fibrin gels may develop capillary tube structure spontaneously and that GECs covered by fibrin gels may undergo disorganization. These GEC phenotype changes are probably both mediate
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