CD86
巨噬细胞极化
脐静脉
小发夹RNA
脂多糖
转染
基因敲除
血管内皮生长因子
化学
流式细胞术
下调和上调
肿瘤坏死因子α
分子生物学
巨噬细胞
免疫学
生物
癌症研究
免疫系统
体外
细胞凋亡
血管内皮生长因子受体
T细胞
基因
生物化学
作者
Yuling Zou,Weiwei Chen,Jia Chen,Zhipeng You
标识
DOI:10.1166/jbn.2022.3469
摘要
Purpose: To explore the impact of VEGF pathway on the M1 polarization and function of macrophages. Methods: VEGFR-knockdown macrophages were established by transfected with a shRNA. M1 macrophages were stimulated by LPS and IFN- γ , which was identified using the flow cytometry. Subsequently, M1 macrophages were treated with VEGF A, VEGF B, and PIGF, respectively. The expression level of iNOS, TNF- α , and IL-6 was detected utilizing RT-PCR. CD86 and iNOS level were checked by Western blot. The migration of HUVEC was evaluated by wound healing assay. Results: The percentage of F4/80 + CD86 + macrophages was significantly elevated by the transfection of shRNA, accompanied by a significantly upregulated expression of CD86 and iNOS. After the stimulation of LPS and IFN- γ , CD86 and iNOS was dramatically upregulated in both the Lv-NC group and Lv-shVEGFR1 group. IL-6 and iNOS levels were greatly declined in macrophages co-treated with LPS, IFN- γ , and PIGF. No marked alterations on the healing degree were noticed in HUVEC stimulated by the supernatant of LPS/IFN- γ treated macrophages, which was dramatically declined by the knockdown of VEGFR1. Conclusion: VEGFR1 facilitated the effect of macrophages on HUVEC migration by regulating the M1 polarization.
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