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目的探讨汉坦病毒(HV)感染后β3整合素与血管内皮生长因子受体2(VEGFR2)的变化及其对内皮功能的影响。方法本研究以体外培养的人脐静脉内皮细胞(HUVEC)为对象,应用黏附试验、Transwell技术及流式细胞技术,观察HV感染后HUVEC黏附和迁移能力的变化,分析β3整合素与VEGFR2在其中的作用及二者表达数量的变化。结果 HV明显抑制HUVEC黏附和迁移能力(P<0.05)。VEGF促进内皮细胞的黏附和迁移的能力可被β3整合素拮抗剂或HV感染所阻断(P<0.05),VEGF促进β3整合素表达的作用也可被HV抑制(P<0.05)。HV可以促进β3整合素及VEGFR2的表达(P<0.05),且二者呈密切正相关(r=0.846)。结论 HV感染对β3整合素、VEGFR2的功能及表达数量的影响可能是其致病机制之一。
Objective To investigate the changes of β3 integrin and vascular endothelial growth factor receptor 2 (VEGFR2) after Hantavirus (HV) infection and their effects on endothelial function. Methods In this study, human umbilical vein endothelial cells (HUVECs) were cultured in vitro. Adhesion test, Transwell technique and flow cytometry were used to observe the changes of HUVEC adhesion and migration after HV infection. The effects of β3 integrin and VEGFR2 The role of both the number of changes and expression. Results HV significantly inhibited the adhesion and migration of HUVECs (P <0.05). The ability of VEGF to promote endothelial cell adhesion and migration could be blocked by β3 integrin antagonist or HV infection (P <0.05). The effect of VEGF on β3 integrin expression was also inhibited by HV (P <0.05). HV can promote the expression of β3 integrin and VEGFR2 (P <0.05), and the two are closely related (r = 0.846). Conclusion The influence of HV infection on the function and expression of β3 integrin and VEGFR2 may be one of the pathogenic mechanisms.