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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Dysfunctional, pro-inflammatory HDL directly upregulates monocyte PDGFRbeta, chemotaxis and TNFalpha production.
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Dysfunctional, pro-inflammatory HDL directly upregulates monocyte PDGFRbeta, chemotaxis and TNFalpha production.

机译：功能异常的促炎性HDL直接上调单核细胞PDGFRbeta，趋化性和TNFalpha的产生。

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摘要

Accelerated atherosclerosis is a major co-morbid condition in autoimmune diseases. Monocytes are the main immune cell involved in atherosclerosis initiation. We hypothesized that dysfunctional, pro-inflammatory HDL (piHDL), which occurs in approximately half of SLE patients, might directly influence monocyte gene expression and function. SLE subjects were stratified into three groups: 1) carotid artery plaque+piHDL+,2) plaque-piHDL+,and 3) plaque-piHDL- (n=18/group). PDGFRbeta was upregulated in primary monocytes from plaque+piHDL+patients and in THP-1 cells acutely treated in vitro with piHDL compared to normal HDL. THP-1 chemotaxis was enhanced after treatment with piHDL versus normal HDL. Abnormal migration was restored to normal levels by treatment with imatinib or an apoJ mimetic peptide. Increased piHDL-mediated TNFalpha protein levels were reduced with both inhibitors. Dysfunctional piHDL directly influences expression of a small number of transcripts and proteins, and piHDL inhibition through reducing piHDL oxidation or blocking PDGFRbeta kinase activity restored normal monocyte chemotaxis.
机译：加速的动脉粥样硬化是自身免疫疾病的主要合并症。单核细胞是参与动脉粥样硬化起始的主要免疫细胞。我们假设功能失调的促炎性HDL（piHDL）发生在大约一半的SLE患者中，可能直接影响单核细胞基因的表达和功能。 SLE受试者分为三组：1）颈动脉斑块+ piHDL +，2）斑块-piHDL +，和3）斑块-piHDL-（n ＝ 18 /组）。与正常的HDL相比，用piHDL在体外急性处理过的斑块+ piHDL +患者的原代单核细胞和PDH-1细胞中的PDGFRbeta上调。用piHDL治疗后，THP-1趋化性比正常HDL增强。通过伊马替尼或apoJ模拟肽治疗，异常迁移恢复到正常水平。两种抑制剂均可降低piHDL介导的TNFα蛋白水平。功能异常的piHDL直接影响少量转录物和蛋白质的表达，并且通过减少piHDL氧化或阻断PDGFRbeta激酶活性来抑制piHDL，恢复了正常的单核细胞趋化性。

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