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    黄巍峰, 李黎, 卿海洋, 黄浩, 方德鹏, 杨渊. 富血小板血浆来源的外泌体通过维持Furin介导的ALK1/ALK5平衡促进软骨细胞增殖并抑制凋亡[J]. 徐州医科大学学报, 2021, 41(12): 881-887. DOI: 10.3969/j.issn.2096-3882.2021.12.004
    引用本文: 黄巍峰, 李黎, 卿海洋, 黄浩, 方德鹏, 杨渊. 富血小板血浆来源的外泌体通过维持Furin介导的ALK1/ALK5平衡促进软骨细胞增殖并抑制凋亡[J]. 徐州医科大学学报, 2021, 41(12): 881-887. DOI: 10.3969/j.issn.2096-3882.2021.12.004
    shu
    Platelet-rich plasma-derived exosomes promote chondrocyte proliferation and inhibit apoptosis by maintaining Furin-mediated ALK1/ALK5 balance[J]. Journal of Xuzhou Medical University, 2021, 41(12): 881-887. DOI: 10.3969/j.issn.2096-3882.2021.12.004
    Citation: Platelet-rich plasma-derived exosomes promote chondrocyte proliferation and inhibit apoptosis by maintaining Furin-mediated ALK1/ALK5 balance[J]. Journal of Xuzhou Medical University, 2021, 41(12): 881-887. DOI: 10.3969/j.issn.2096-3882.2021.12.004
    shu

    富血小板血浆来源的外泌体通过维持Furin介导的ALK1/ALK5平衡促进软骨细胞增殖并抑制凋亡

    Platelet-rich plasma-derived exosomes promote chondrocyte proliferation and inhibit apoptosis by maintaining Furin-mediated ALK1/ALK5 balance

      摘要
    • 摘要: 目的：探讨富含血小板血浆（PRP）来源外泌体（PRP-Exo）对体外白介素1β（IL-1β）处理的软骨细胞的保护作用和分子机制。方法：exoEasy Maxi 试剂盒分离和纯化PRP-Exo，并进行鉴定和表征。在大鼠软骨细胞中加入IL-1β模拟体外骨关节炎（OA）的软骨细胞（IL-1β组）。并在IL-1β基础上，使用PRP-Exo（IL-1β+PRP-Exo组）和PRP-As（IL-1β+PRP-As组）治疗，使用CCK-8法检测细胞增殖和流式细胞术检测细胞凋亡，从而比较PRP-Exo和活化PRP（PRP-As）处理的效果。通过Western blot和qRT-PCR分析涉及Furin介导ALK1/ALK5信号平衡的机制。结果：成功从PRP分离纯化了外泌体。IL-1β+PRP-As组和IL-1β+PRP-Exo组的肿瘤坏死因子-α（TNF-α）水平和细胞凋亡率低于IL-1β组，细胞增殖率和Furin的水平均高于IL-1β组（均P＜0.05），而且IL-1β+PRP-Exo组在促进软骨细胞增殖并抑制凋亡作用都优于IL-1β+PRP-As组（均P＜0.05）。软骨细胞中加入Furin可明显降低ALK1/ALK5比率（P＜0.05）。IL-1β不仅降低软骨细胞中Furin水平，而且增加ALK1/ALK5的比率（均P＜0.05），而加入PRP-Exo可通过增加Furin水平从而降低ALK1/ALK5比率（均P＜0.05）。结论：PRP-Exo通过维持Furin介导的ALK1/ALK5平衡促进软骨细胞增殖并抑制凋亡。

       

      Abstract: ob＜x＞jective: To investigate the protective effect and molecular mechanism of platelet rich plasma (PRP) -derived exosome (PRP-exo) on interleukin-1β (IL-1β) treated chondrocytes in vitro.METHODS: PrP-Exo was isolated and purified with ExoEasy Maxi kit, and then identified and characterized. Rat chondrocytes were cultured and IL-1β was added to simulate in vitro osteoarthritis (OA) chondrocytes (IL-1β group).On the basis of IL-1β, PRP-Exo (IL-1β+PRP-Exo group) and PRP-As (IL-1β+PRP-Exo group) were used for treatment, cell proliferation was detected by CCK-8 assay and apoptosis was detected by flow cytometry to compare the effects of PRP-Exo and activated PRP (PRP-As group).Western blot analysis and qRT-PCR analysis involved the mechanism of Furin-mediated ALK1/ALK5 signal balance.Results: Exosomes were successfully isolated and purified from PRP.Tumor necrosis factor-α (TNF-α) level and cell apoptosis rate in IL-1β+ Prp-As and IL-1β+ Prp-Exo groups were lower than those in IL-1β group, while cell proliferation rate and Furin level were higher than those in IL-1β group (all P < 0.05).Moreover, the effect of IL-1β+ PrP-Exo group was better than that of IL-1β+ PrP-As group (all P < 0.05).Adding Furin to chondrocytes significantly decreased the ALK1/ALK5 ratio (P < 0.05).IL-1β not only decreased the level of Furin in chondrocytes, but also increased the ratio of ALK1/ALK5 (all P < 0.05), while PRP-Exo could decrease the ratio of ALK1/ALK5 by increasing the level of Furin (all P < 0.05).Conclusion: PRP-Exo can promote chondrocyte proliferation and inhibit apoptosis by maintaining Furin-mediated ALK1/ALK5 balance

       

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