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2025 02 v.41 72-79
类风湿关节炎滑液来源的细胞外囊泡促进HUVEC血管生成
基金项目(Foundation): 国家自然科学基金(32060178); 宁夏自然科学基金(2024AAC03257)
邮箱(Email): hanmei0708@126.com;
DOI: 10.13431/j.cnki.immunol.j.20250010
中文作者单位:

宁夏医科大学基础医学院病原生物学与医学免疫学系;国龙骨科医院骨科;咸阳职业技术学院;

摘要(Abstract):

目的 探讨类风湿关节炎(RA)患者膝关节滑液中的细胞外囊泡(EVs)对脐静脉内皮细胞血管生成的影响并初步探讨其机制。方法 收集20例RA患者膝关节滑液,以20例骨关节炎(OA)患者的滑液为对照。采用差速超速离心法纯化EVs,用透射电镜和纳米颗粒追踪观察分析EVs的形态和大小。通过Western blot检测EVs的CD9、CD63、细胞色素C (Cyt-c),及所含血管内皮细胞生长因子(VEGF)、赖氨酰氧化酶(LOX)、基质金属蛋白酶2(MMP2)、肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)水平。用2种EVs干预人脐静脉内皮细胞(HUVEC),分别以CCK8法、TranswellTM小室试验、细胞划痕实验和Matrigel胶血管生成试验检测HUVEC增殖、迁移和血管生成。用Western blot检测EVs干预对HUVEC中PI3K/AKT通路的影响。结果 RA滑液来源的EVs(RA-EVs)和OA滑液来源的EVs(OA-EVs)均呈杯口状,直径在30~400 nm之间,表达CD63和CD9,不表达Cyt-c。RA-EVs中所携带的VEGF、LOX、MMP2、TNF-α和TGF-β1较OA-EVs多。与OA-EVs干预组相比,RA-EVs显著促进HUVEC增殖、迁移和血管生成,上调PI3K/AKT的磷酸化,而PI3K抑制剂能够抑制EVs诱导的血管生成。结论RA关节滑液中的EVs携带较多的促血管生成和炎症相关的细胞因子和酶,可通过激活PI3K/AKT通路促进血管生成,参与RA病理进展。

关键词(KeyWords): 类风湿关节炎;细胞外囊泡;血管生成;滑液;人脐静脉内皮细胞
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基本信息:

DOI:10.13431/j.cnki.immunol.j.20250010

中图分类号:R593.22

引用信息:

[1]王凯博,徐传皓,田彦斌等.类风湿关节炎滑液来源的细胞外囊泡促进HUVEC血管生成[J].免疫学杂志,2025,41(02):72-79.DOI:10.13431/j.cnki.immunol.j.20250010.

基金信息:

国家自然科学基金(32060178); 宁夏自然科学基金(2024AAC03257)

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