J Periodontol:富含血小板纤维蛋白/双向性磷酸钙通过内在线粒体通路减弱慢性牙周炎内的破骨细胞分化并促进凋亡

2018-07-21 lishiting MedSci原创

这篇研究通过获取慢性牙周炎(CP)患者外周血来源的破骨细胞,评估PRF/BCP对其分化和存活的影响。

这篇研究通过获取慢性牙周炎(CP)患者外周血来源的破骨细胞,评估PRF/BCP对其分化和存活的影响。研究提取25名CP患者及25名健康个体的外周血单核细胞(PBMCs),检测其分化抗原14+(CD14+)的表达,并施加巨噬细胞集落刺激因子(M-CSF)和核因子-κB配体的受体激活剂 (RANKL) 刺激,体外诱导单核细胞向破骨细胞分化21天。随后通过抗酒石酸酸性磷酸酶(TRAP)检测破骨细胞数量。通过检测Bcl-2, Bax, Bcl-xL, 活化B细胞的核因子κ-轻链增强子(NF-κB), caspase 3/9和脱氧核糖核酸(DNA)片段检测凋亡的机制。结果显示,与对照组(健康个体)相比,测试组循环破骨细胞的比例相对增加。另外,未施加刺激的CP细胞中的破骨细胞前体比施加PRF/BCP的细胞更具有破骨分化性。因此,CP细胞中的破骨细胞数量显著增加。施加PRF/BCP刺激的CP细胞中,转录因子NF-κB受到直接抑制,而caspase 3/9水平和caspase 3活性明显增加。此外,施加PRF/BCP 促使Bax的蛋白表达和转录活性上调和Bcl-2和Bcl-xL水平下调。结论:结果表明

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    2019-02-01 feather89
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  5. 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  6. 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    2018-07-23 jj000004
  7. 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  8. 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GetPortalCommentsPageByObjectIdResponse(id=333225, encodeId=7abd3332255d, content=好好学习,天天向上。, beContent=null, objectType=article, channel=null, level=null, likeNumber=83, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://cdnapi.center.medsci.cn/medsci/head/2018/07/16/3b24606172648eea459125cb74754afe.jpg, createdBy=6c022216608, createdName=liumin1987, createdTime=Sun Jul 22 00:03:27 CST 2018, time=2018-07-22, status=1, ipAttribution=)]
    2018-07-22 清风拂面

    谢谢分享学习

    0

  9. 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    2018-07-22 yjs木玉

    学习学习学习

    0

  10. 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content=谢谢分享学习, beContent=null, objectType=article, channel=null, level=null, likeNumber=92, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://wx.qlogo.cn/mmopen/Q3auHgzwzM4o2XVpJ6449yqDsjibydI5HnJ8MibGxNn4HZiaZib0bdfibbwoz3KQrIyN9AGxq36ZlZRNicYlPfOOWMtwgsajY6mGNFiaPclFdowjD0/0, createdBy=97bd1338592, createdName=清风拂面, createdTime=Sun Jul 22 12:22:52 CST 2018, time=2018-07-22, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=333262, encodeId=61d733326241, content=学习学习学习, beContent=null, objectType=article, channel=null, level=null, likeNumber=89, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://cdnapi.center.medsci.cn/medsci/head/2017/08/29/bbc5cc0eed9b8d17623d2fd49dbdf19a.jpg, createdBy=79522135794, createdName=yjs木玉, createdTime=Sun Jul 22 06:05:34 CST 2018, time=2018-07-22, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=333225, encodeId=7abd3332255d, content=好好学习,天天向上。, beContent=null, objectType=article, channel=null, level=null, likeNumber=83, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=https://cdnapi.center.medsci.cn/medsci/head/2018/07/16/3b24606172648eea459125cb74754afe.jpg, createdBy=6c022216608, createdName=liumin1987, createdTime=Sun Jul 22 00:03:27 CST 2018, time=2018-07-22, status=1, ipAttribution=)]
    2018-07-22 liumin1987

    好好学习,天天向上。

    0

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破骨细胞是负责骨吸收的大型多核细胞。破骨细胞的过度炎症活化导致骨侵蚀,是几种疾病如类风湿性关节炎(RA)的标志。盐诱导型激酶(SIK)构成包含三个成员(SIK1,-2和-3)的激酶亚科。在巨噬细胞中抑制SIK激酶活性可诱导抗炎表型。由于破骨细胞起源于巨噬细胞来源的前体,研究人员假设SIK在破骨细胞发生中发挥作用。研究使用小鼠巨噬细胞细胞系RAW264.7和骨髓来源的巨噬细胞(BMM)分析了SIK1

J Nanosci Nanotechnol:磷酸钙硅酸盐和硅酸钙水泥可有效抑制破骨细胞的活性

磷酸钙骨水泥(CPSC)可刺激成骨细胞增殖并促进成骨,但CPSC如何通过细胞因子调节抑制破骨细胞活性尚不清楚。在目前的研究中,我们通过将磷酸一钙(MCP)掺入硅酸钙水泥(CSC)中来合成CPSC,并分析了CSC和CPSC对破骨细胞存活与MTT的影响。我们发现CSC和CPSC培养基均可降低破骨细胞活性,流式细胞术进一步表明CSC和CPSC可抑制破骨细胞活性。为了阐明潜在的机制,评估了与破骨细胞活性相

Ann Rheum Dis:非经典型单核细胞是关节炎组织破坏的介质

非经典型单核细胞是关节炎组织损伤的关键细胞,也是预防炎性关节损伤的潜在治疗靶点。

Epigenetics:组蛋白去甲基化酶KDM4B可抑制破骨细胞的生成

牙周病(PD)困扰46%的美国人,目前没有有效的辅助疗法。尽管PD的大多数药物治疗靶,但宿主免疫应答是导致组织损伤和骨质丧失的主要原因。本研究中,我们确定组蛋白去甲基化酶KDM4B是用于治疗PD的潜在药物靶标。免疫组织化学染色显示患病牙周上皮KDM4B丰度增加,与炎症相关。在暴露于伴放线聚集杆菌脂多糖(Aa-LPS)的小鼠颅骨切片中,免疫组织化学染色显示KDM4B蛋白表达明显增加。已知8-羟基喹啉

Oncogene:MacroH2A1.2能够抑制前列腺癌诱导的破骨细胞的形成

破骨细胞是多核的具有骨再吸收活性的细胞,并且分化自造血干细胞。前列腺癌细胞能够频繁的扩展到骨组织并且分泌可溶性的信号分子来刺激破骨细胞的分化和骨质吸收。然而,前列腺癌细胞分泌的破骨细胞形成的可溶性因子的表达过程及机制仍旧不清楚。MacroH2A1.2(mH2A)是一个组蛋白变体,在特定的基因组位点能够替代H2A,并且能够建立具有功能性差异的染色质区域。最近,有研究人员报道了 mH2A1.2,一种m