Fractalkine对类风湿关节炎成纤维样滑膜细胞增殖的影响

目的明确fractalkine(CX3CL1)对人类风湿关节炎成纤维样滑膜细胞(RA-FLS)增殖的影响。方法通过组织块法培养RA-FLS。分别用0、50、100ng/mL重组人fractalkine刺激RA-FLS24h,用四唑盐(MTT)法检测其吸光度值,比较各组间增殖率。结果 50ng/ml及100ng/ml fractalkine均可促进RA-FLS增殖(P=0.005,P=0.022)。结论 Fractalkine可促进RA-FLS的增殖,可部分解释RA-FLS自主增殖的特性。     

STF-31对类风湿关节炎成纤维样滑膜细胞增殖和凋亡影响的机制分析

目的 观察STF?31对类风湿关节炎成纤维样滑膜细胞(RAFLs)的增殖以及凋亡的作用并分析其机制。方法 应用2μmol/L、4μmol/L、8μmol/L浓度的STF?31处理RAFLs,并设置一组不加STF?31的空白对照。分别于24 h、48 h以及72 h进行下述指标观察：以MTT法检测STF?31对RAFLs细胞的增殖抑制效果;通过倒置显微镜观察STF?31作用后的细胞形态学改变;以ATP试剂盒分析STF?31作用后的RAFLs细胞内ATP水平;通过JC?1得到给药后RAFLs内线粒体膜电位的变化;以流式细胞术双染法观察STF?31作用于RAFLs细胞48 h后产生的细胞凋亡比率;应用Western blot法检测STF?31作用在RAFLs后的凋亡相关蛋白Bax、Bcl?2以及p?Akt的表达。结果 STF?31随着浓度增加、时间延长,可以更好地抑制RAFLs细胞的增殖(P<0.05),作用RAFLs细胞24 h、48 h和72 h的IC₅₀分别为9.870、1.400和0.513μmol/L;镜下观察到STF?31作用在RAFLS细胞后,RAL...     

周期性机械拉伸对类风湿关节炎成纤维样滑膜细胞增殖的影响

目的探讨周期性机械拉伸对类风湿关节炎成纤维样滑膜细胞(RA-FLSs)增殖能力的影响。方法实验组细胞在周期性机械拉伸频率为1.0 Hz、拉伸幅度为3%、6%和9%的条件下,分别对RA-FLSs加载2、6和12 h。对照组细胞在保持与实验组培养条件一致的情况下不进行拉伸刺激。机械拉伸后,用流式细胞术和MTS检测细胞的增殖和活性。RT-PCR检测加载后细胞周期调控因子(CyclinD1、CyclinE1、CDK2、P27)在基因水平上的表达变化。结果 6%和9%的拉伸刺激持续作用6、12 h使RA-FLSs增殖和活性显著降低(P<0.05),同时CDK2和CyclinE1的mRNA表达降低,P27 mRNA的表达增高(P<0.05),周期性机械拉伸对CyclinD1表达的影响相对较小。结论周期性机械拉伸对RA-FLSs增殖能力的影响与拉伸强度以及持续的时间有关,6%和9%的机械拉伸刺激可以抑制RA-FLSs的增殖,而这种增殖抑制作用可能是通过调控CyclinE1,CDK2和P27的表达来实现的。本研究对于探讨力学刺激在类风湿性关节炎的发病机制以及临床防治中的作用具有一定意义。     

IL-32γ对类风湿关节炎成纤维样滑膜细胞增殖与细胞周期的影响

目的:研究IL-32γ对类风湿关节炎(RA)成纤维样滑膜细胞(FLS)增殖与细胞周期的影响及机制。方法:体外培养活动性类风湿关节炎和骨关节炎(OA)患者成纤维样滑膜细胞并以IL-32γ处理,应用MTT法检测细胞增殖;流式细胞术检测细胞周期;Western印迹方法检测cyclinD1及NF-κBp65蛋白含量;免疫细胞化学染色法检测PCNA表达的变化。结果:IL-32γ对OA-FLS增殖没有影响;不同浓度的IL-32γ(10～100 ng/ml)在72～120小时范围内,浓度和时间依赖性促进RA-FLS增殖;100 ng/ml的IL-32γ作用RA-FLS 48小时后促进了细胞周期由G1期向S期,进而G2/M期转化,同时上调了cyclin D1、NF-κBp65和PCNA的蛋白表达水平。结论:IL-32γ可促进RA-FLS增殖和加速细胞周期转化。上调NF-κBp65和cyclin D1的表达可能是其作用机制之一。     

RICTOR对类风湿关节炎成纤维样滑膜细胞活力的影响

 目的：通过siRNA介导的RNA干扰技术沉默类风湿关节炎（RA）成纤维样滑膜细胞（FLS）mTORC2的特异组成蛋白RICTOR的表达,观察其对细胞活力的影响。方法：组织块法培养RA-FLS。应用阳离子脂质体转染的方法,把化学合成的特异性RICTOR siRNA转染RA-FLS,并以转染非特异性siRNA作为阴性对照。利用荧光定量PCR法分析转染24 h后细胞RICTOR mRNA表达水平的变化;Western blotting法分析转染48和72 h后细胞RICTOR蛋白表达水平的变化;以噻唑蓝（MTT）比色法检测转染成纤维样滑膜细胞不同时间（24、48和72 h）RICTOR siRNA对细胞活力的影响。结果：荧光定量PCR结果显示特异性RICTOR siRNA转染组与对照组相比,细胞中RICTOR的mRNA表达水平显著下调,24 h干扰效率达78.3%±63.71%（P<0.01）。Western blotting结果显示与对照组相比,RICTOR siRNA转染组48 h和72 h后RICTOR蛋白表达水平明显降低,沉默效率分别为92.48%±6.14%和98.57%±1.40%（均P<0.01）。MTT结果显示,早期（24和48 h）RICTOR siRNA转染组与阴性对照组细胞存活率比较无显著差异;72 h后,RICTOR siRNA转染组与阴性对照相比,细胞活力明显降低,抑制率为90.14%±1.90%（P<0.01）。结论：转染特异性RICTOR siRNA可降低RA-FLS的活力,提示mTORC2可能与RA-FLS的生长有关。     

lncRNA LINC01419 靶向 miR-320a 对小儿类风湿关节炎滑膜成纤维细胞增殖、迁移和侵袭的影响

目的：探讨lncRNA LINC01419对小儿类风湿关节炎滑膜成纤维细胞增殖、迁移和侵袭的影响及分子机制。方法：取2017年1月至2019年12月本院21例小儿类风湿关节炎患者的滑膜组织及21例因骨折式创伤截肢者的膝关节正常滑膜组织;分离培养小儿类风湿关节炎滑膜成纤维细胞（RASFs）,将其分为si-NC组、si-LINC01419组、pcDNA组、pcDNALINC01419组、miR-NC组、miR-320a组、si-LINC01419+anti-miR-NC组、si-LINC01419+anti-miR-320a组。实时荧光定量PCR(RT-qPCR)检测LINC01419和miR-320a的表达水平;四甲基偶氮唑盐比色法（MTT）检测细胞活性;Transwell检测细胞迁移和侵袭;Western blot法检测细胞周期蛋白D1(CyclinD1)、细胞周期蛋白依赖性激酶抑制剂1A(p21)、基质金属蛋白酶2(MMP-2)、基质金属蛋白酶9(MMP-9)蛋白表达;荧光素酶报告实验检测LINC01419和miR-320a的靶向关系。结果：与正常滑膜组织相比,小儿类风湿关节炎患者滑...     

沉默TREM-2对类风湿关节炎成纤维样滑膜细胞迁移和侵袭的影响

 目的: 应用RNA干扰(RNAi)技术沉默类风湿关节炎成纤维样滑膜细胞(RA-FLS)髓样细胞触发受体2(TREM-2)的表达,探讨TREM-2基因沉默对RA-FLS迁移和侵袭能力的影响及其相关机制。方法: 向RA-FLS转染特异性的TREM-2 siRNA,利用RT-PCR法和Western blot法检测沉默效果;CCK-8法检测各组细胞生长情况;Transwell小室测定细胞的迁移和侵袭能力;ELISA法检测细胞MMP-2和MMP-9的分泌水平;Western blot法分析沉默TREM-2基因对细胞PI3K/AKT通路的影响。结果: TREM-2 siRNA能显著降低RA-FLS中TREM2 mRNA和蛋白的表达(P<0.05)。沉默TREM-2基因后,各时点各组细胞的活力未见明显差异;特异性干扰组RA-FLS的迁移细胞数目与空白组和control siRNA组相比明显增多(P<0.05);TREM-2 siRNA组侵袭细胞数目相比空白组和control siRNA组明显增多(P<0.05);TREM-2 siRNA干扰后RA-FLS分泌的MMP-2显著增加(P<0.05)而MMP-9未见明显变化;特异性转染后的RA-FLS相对于对照组PI3K/AKT的磷酸化水平显著增强(P<0.05)。结论: TREM-2可能通过调节PI3K/AKT通路的活化对RA-FLS的迁移和侵袭能力发挥着重要作用。     

TL1A促进类风湿关节炎患者成纤维样滑膜细胞分泌PGE_2

为了探讨肿瘤坏死因子样配体1A(TL1A)对类风湿关节炎(RA)患者成纤维样滑膜细胞(FLS)分泌前列腺素E2(PGE2)的影响,分离培养6例RA FLS,并分别用TL1A、肿瘤坏死因子受体(TNFR)拮抗剂(0.25μg/ml)加TL1A(50ng/ml)以及信号通路抑制剂(10μmol/L)加TL1A(50ng/ml)刺激。采用反转录聚合酶链式反应(RT-PCR)检测RA FLS Cox-2mRNA的表达;采用酶联免疫吸附试验(ELISA)检测RA FLS培养上清液中PGE2的水平。统计学方法采用t检验。结果显示,与未刺激组相比,TL1A刺激的RA FLS Cox-2mRNA和PGE2表达均增多(P0.05);加入TNFR2拮抗剂可使TL1A刺激的RA FLS分泌PGE2水平显著降低(P0.05)。此外,细胞培养体系加入NF-κB和JNK抑制剂后,TL1A刺激RA FLS产生PGE2水平明显下降(P0.05)。研究表明,TL1A与TNFR2结合可能通过NF-κB和JNK信号通路促进RA FLS分泌PGE2,参与RA的发病过程。     

IL-22对类风湿关节炎成纤维样滑膜细胞的作用

目的:探究白细胞介素(IL)-22对类风湿关节炎(RA)成纤维样滑膜细胞(FLSs)功能的影响及机制。方法:组织块法培养RA-FLSs。将不同浓度(0、1、10、100μg/L)的重组人源性IL-22(rhIL-22)与RA-FLSs共培养24 h、48 h、72 h,CCK-8法检测细胞活力的改变;利用10μg/L的rhIL-22作用于RA-FLSs 24 h,流式细胞术检测细胞周期改变。rhIL-22和/或信号转导和转录因子3(STAT3)特异性抑制剂STA-21以不同浓度作用RA-FLSs 24h,Western blot法检测Bcl-2和p-STAT3蛋白水平的变化。结果:不同浓度的rhIL-22作用于RA-FLSs 24 h、48 h、72h后,RA-FLSs细胞活力明显增高,均显著高于对照组(P0.05)。rhIL-22刺激RA-FLSs后,S期和G_2/M期细胞明显增多,G_0/G_1期细胞减少。Western blot法检测结果提示rhIL-22可上调RA-FLSs中Bcl-2、p-STAT3的蛋白水平,而STA-21单用或联用rhIL-22均可抑制RA-FLSs中Bcl-2及p-STAT3的表达(P0.05)。结论:IL-22在RA-FLSs细胞活力和周期调节中起重要作用,且STAT3在IL-22促RA-FLSs细胞Bcl-2表达的过程中起关键作用,提示IL-22可能对RA-FLSs凋亡有一定的影响。     

PTEN在类风湿关节炎成纤维样滑膜细胞中的表达及意义

目的:探讨第10号染色体缺失的磷酸酶及张力蛋白同源基因(PTEN)在人类风湿关节炎(RA)成纤维样滑膜细胞(FLS)中的表达水平及意义。方法:利用组织块法获得并体外培养人RA-FLS、骨关节炎(OA)-FLS及关节创伤-FLS;采用实时荧光定量PCR法检测各组FLS中PTEN mRNA表达水平的差异;采用Western blotting法检测各组FLS的PTEN蛋白表达水平以及Akt Thr308位点磷酸化水平的差异。结果:(1)RA-FLS中的PTEN mRNA表达水平显著低于OA-FLS及关节创伤-FLS(P0.01),而OA-FLS与关节创伤-FLS之间的PTEN mRNA表达水平无统计学差异。(2)RA-FLS的PTEN蛋白表达水平显著低于OA-FLS及关节创伤-FLS(P0.05),而OA-FLS与关节创伤-FLS之间的PTEN蛋白表达水平无统计学差异。(3)RA-FLS中的Akt蛋白Thr308位点磷酸化水平显著高于OA-FLS及关节创伤-FLS(P0.01),且OA-FLS中该位点的磷酸化水平显著低于关节创伤-FLS(P0.01)。(4)RA-FLS中的PTEN蛋白水平与Akt Thr308位点磷酸化水平呈显著负相关(P0.01)。结论:RAFLS中PTEN基因呈低水平表达,可能与Akt Thr308位点磷酸化水平异常增高相关。     

Roles of claudin-5 and von Willebrand factor in patients with rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic inflammatory disorder that affects approximately 1% of the world’s population. The pathogenesis of RA is not understood fully. It is assumed that endothelial function is associated with the proinflammatory state of RA. Endothelial dysfunction/activation reflects the increased level of von Willebrand factor (vWF) and a shift toward prothrombotic activity of the endothelium. The present study was performed to investigate the possible relationships between vWF and claudin-5 and the level of disease activity in patients with RA. The study population was divided into four groups according to the disease activity score in 28 joints (DAS28): remission group (RG), 18 patients (DAS28 < 2.6); low disease activity group (LDAG), 23 patients (DAS28 > 2.6-3.2); moderate disease activity (MDAG), 23 patients (DAS28 > 3.2-5.1); high disease activity group (HDAG), 14 patients (DAS28 > 5.1); and control group (CG), 10 healthy subjects. Claudin-5 and vWF assessment were derived from serum samples gathered from the patients known to have RF and anti-CCP titers in the normal ranges. A high positive association of claudin-5 and vWF with the MDAG was observed (P < 0.001). The results of our study indicated that the relationship between vWF and claudin-5, which are indicators of endothelial cell dysfunction and tight junction activity, may be a predictor of disease activity. Further studies are required to investigate these pathways to shed light on the roles of claudin-5 and vWF in the progression of inflammation and other vascular conditions.     

类风湿关节炎大鼠滑膜细胞的类肿瘤样增生与相关基因表达的关系

目的:探讨佐剂性关节炎(AA)大鼠滑膜细胞的类肿瘤样增生和相关基因表达的机制。方法:将Wistar大鼠随机分两组,每组10只,并应用弗氏完全佐剂诱发大鼠AA实验性模型,定期观测踝关节肿胀度至第40天。分别取AA模型组和正常对照组大鼠踝关节进行组织切片,用HE染色后观察病理学变化。取大鼠膝关节滑膜组织体外进行原代细胞培养,用MTT比色法检测大鼠滑膜细胞的增生。同时采用RTPCR法,检测模型组及正常对照组大鼠滑膜组织中相关基因Cmyc和ODCmRNA的转录水平。结果:①体外培养的AA模型组大鼠关节滑膜细胞的增殖显著高于正常组大鼠(P<0.01),并呈类肿瘤样增生。②AA模型组大鼠关节滑膜组织中,Cmyc和ODCmRNA的转录水平明显高于正常对照大鼠(P<0.01)。结论:AA模型组大鼠关节滑膜细胞的类肿瘤样增生,可能与其相关基因Cmyc和ODCmRNA的转录水平增高有关。     

Combination of nifedipine and subtherapeutic dose of cyclosporin additively suppresses mononuclear cells activation of patients with rheumatoid arthritis and normal individuals via Ca(2+) -calcineurin-nuclear factor of activated T cells pathway

Abnormal Ca²⁺‐mediated signalling contributes to the pathogenesis of rheumatoid arthritis (RA). However, the potential implication of calcium channel blocker in RA remained unknown. We hypothesized that nifedipine, an L‐type calcium channel blocker, combined with a calcineurin inhibitor, could suppress T cell activation via targeting different level of the Ca²⁺ signalling pathway. The percentage of activated T cells and the apoptotic rate of mononuclear cells (MNCs) was measured by flow cytometry. The MNC viability, cytokine production, cytosolic Ca²⁺ level and activity of the nuclear factor of activated T cells (NFAT) were measured by enzyme‐linked immunosorbent assay (ELISA). The NFAT‐regulated gene expression, including interleukin (IL)‐2, interferon (IFN)‐γ and granulocyte–macrophage colony‐stimulating factor (GM‐CSF), was measured by real‐time polymerase chain reaction (PCR). We found that the percentage of activated T cells in anti‐CD3 + anti‐CD28‐activated MNC was higher in RA patients. High doses of nifedipine (50 µM) increased MNCs apoptosis, inhibited T cell activation and decreased T helper type 2 (Th1) (IFN‐γ)/Th2 (IL‐10) cytokine production in both groups. The Ca²⁺ influx was lower in anti‐CD3 + anti‐CD28‐activated MNC from RA patients than healthy volunteers and suppressed by nifedipine. When combined with a subtherapeutic dose (50 ng/ml) of cyclosporin, 1 µM nifedipine suppressed the percentage of activated T cells in both groups. Moreover, this combination suppressed more IFN‐γ secretion and NFAT‐regulated gene (GM‐CSF and IFN‐γ) expression in RA‐MNCs than normal MNCs via decreasing the activity of NFATc1. In conclusion, we found that L‐type Ca²⁺ channel blockers and subtherapeutic doses of cyclosporin act additively to suppress the Ca²⁺‐calcineurin‐NFAT signalling pathway, leading to inhibition of T cell activity. We propose that this combination may become a potential treatment of RA.     

Expression of aquaporin 5 increases proliferation and metastasis potential of lung cancer

Water channel aquaporin 5 (AQP5) is highly expressed at the apical membrane of alveolar type I epithelial cells and confers high osmotic water permeability. AQP5 is also expressed in lung cancer tissue. Previous studies showed there was an up‐regulation of AQP5 expression in cancer tissue compared to surrounding normal tissue. In addition, expression of AQP5 in lung cancer tissue was associated with poor prognosis. Herein, we tested the role of AQP5 in lung cancer oncogenesis and development. Lung cancer cells with different expression of AQP5 were used to study cell proliferation and migration, two important parameters for tumour cell biology. We found enhanced proliferation and migration potential in cancer cells with high AQP5 expression, while reduced proliferation and metastasis potential in cancer cells with low AQP5 expression. Oncogene analysis showed significantly increased PCNA and c‐myc expression in AQP5 transfected cells. AQP5 transfected cells also showed significant increased MUC5AC mucin expression, which might contribute to the enhanced metastasis potential of lung cancer. AQP5 overexpression resulted in enhanced activation of the epidermal growth factor receptor (EGFR), extracellular receptor kinase (ERK1/2), and p38 mitogen‐activated protein kinase (p38 MAPK) pathway in cancer cells. Moreover, deletion of AQP5 demonstrated decreased activation of the EGFR/ERK/p38 MAPK pathway in AQP5 knockout mice lungs, while deletion of AQP1 or AQP3 did not exhibit significant changes on activation of the EGFR/ERK/p38 MAPK pathway in lung tissue. In conclusion, our results provide evidence for AQP5‐facilitated lung cancer cell proliferation and migration, possibly through activation of the EGFR/ERK/p38 MAPK signalling pathway, but why AQP5 but not other aquaporin expression affects the EGFR/ERK/p38 MAPK pathway still needs further exploration. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

miR-455-3p靶向HIPK2调控高糖环境下成骨细胞的增殖和凋亡

文题释义： 糖尿病性骨病：糖尿病可导致骨代谢发生改变,表现为骨形成缺陷、成骨细胞数量减少、骨基质形成不足。高糖环境下以成骨细胞功能改变最为显著,高糖诱导成骨细胞是研究糖尿病性骨病的常用细胞模型。 成骨作用：指成骨细胞移至将要合成骨组织的部位,分泌、合成骨胶原及骨蛋白纤维,将钙、磷吸收到纤维孔隙中进行沉淀结晶,形成骨组织的过程。 背景：以往研究表明多种miRNA在骨形成中发挥作用,miR-335-5p可保护成骨细胞免受氧化应激,对枸橼酸铁铵诱导的成骨细胞具有保护作用,但miR-335-5p对高糖环境下成骨细胞增殖和凋亡的影响尚未可知。 目的：探讨miR-455-3p靶向HIPK2对高糖环境下成骨细胞增殖和凋亡的影响。 方法：双荧光素酶报告基因分析法验证miR-455-3p对HIPK2的靶向作用。体外用高糖诱导MC3T3-E1细胞,分为空白组、高糖组、高糖+miR-control组、高糖+miR-455-3p组、高糖+si-control组、高糖+si-HIPK2组、高糖+miR-455-3p+pcDNA组和高糖+miR-455-3p+pcDNA-HIPK2组。qRT-PCR检测miR-455-3p和HIPK2 mRNA的表达,MTT法检测细胞存活率,流式细胞检测细胞凋亡,Western blot检测HIPK2、p-STAT3和STAT3蛋白的表达。 结果与结论：①HIPK2是miR-455-3p的靶基因,miR-455-3p可负性调控HIPK2的表达;②高糖处理可抑制miR-455-3p的表达,促进HIPK2的表达;③过表达miR-455-3p或抑制HIPK2表达均可促进高糖条件下MC3T3-E1细胞的存活和抑制凋亡;④过表达HIPK2可部分逆转miR-455-3p对高糖条件下成骨细胞的存活促进和凋亡抑制作用;⑤miR-455-3p通过调控HIPK2抑制成骨细胞中p-STAT3的表达;⑥结果表明,miR-455-3p通过靶向下调HIPK2抑制高糖诱导的成骨细胞凋亡,促进成骨细胞增殖,这可能与抑制STAT3信号通路有关。 ORCID: 0000-0001-7129-8455(匡嘉兵) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

miR-145-5p的过表达对乳腺癌细胞凋亡作用的研究

目的 探讨miR-145-5p靶向调控激活转录因子1(ATF1)对人乳腺癌MCF7细胞凋亡的影响.方法 运用TargetScan在线分析miR-145-5p与ATF1的相关性;将ATF1的3'UTR构建进PMIR-RB-REPORT质粒,利用荧光素酶报告实验检测miR-145-5p是否靶向调控ATF1;用HiPerFe...     

Effect of interleukin‐6 receptor blockade on the balance between regulatory T cells and T helper type 17 cells in rheumatoid arthritis patients

A new paradigm has emerged relating the pathogenesis of rheumatoid arthritis (RA), focused on the balance between T helper type 17 cells and regulatory T cells (T_regs). In humans, both subpopulations depend on transforming growth factor (TGF)‐β for their induction, but in the presence of inflammatory cytokines, such as interleukin (IL)‐6, the generation of Th17 is favoured. Tocilizumab is a therapeutic antibody targeting the IL‐6 receptor (IL‐6R), which has demonstrated encouraging results in RA. The aim of this study was to evaluate the effect of tocilizumab on Th1 cells, Th17 cells, IL‐17 and interferon (IFN)‐γ double secretors Th17/Th1 cells, and T_regs in RA patients. Eight RA patients received tocilizumab monthly for 24 weeks and blood samples were obtained every 8 weeks to study T cell populations by flow cytometry. The frequency of Th17 cells, Th1 cells and Th17/Th1 cells was evaluated in peripheral blood mononuclear cells (PBMCs) activated in vitro with a polyclonal stimulus. T_regs were identified by their expression of forkhead box protein 3 (FoxP3) and CD25 by direct staining of PBMCs. Although no changes were detected in the frequency of Th1 or Th17 cells, the percentages of peripheral T_regs increased after therapy. In addition, the infrequent Th17/Th1 subpopulation showed a significant increment in tocilizumab‐treated patients. In conclusion, tocilizumab was able to skew the balance between Th17 cells and T_regs towards a more protective status, which may contribute to the clinical improvement observed in RA patients.     

Expression of CD5 and CD72 on T and B cell subsets in rheumatoid arthritis and Sjögren's syndrome.

A minority of B cells express the CD5 marker, which is found on virtually all T cells, and CD72 has been defined as the CD5 ligand on the B cell membrane. The mean fluorescence intensity (MFI) of the CD5 molecules was shown to be higher on CD4+CD29+ than CD4+CD45RA+ in peripheral blood (PB) and synovial fluid (SF) of rheumatoid arthritis (RA) patients (P < 0.0001 and < 0.001), and PB of Sjögren's syndrome (SS) patients and normal controls (P < 0.02 and < 0.03). This MFI declined once the CD4 expressed HLA-DR in PB of SS patients (P < 0.004) and normal controls (P < 0.02) or CD25 in PB of RA (P < 0.004) and SS patients (P < 0.0004). There was a correlation between the CD5 MFI on CD4+CD45RA+ and CD4+CD29+ in RA (P < 0.001) as well as SS (P < 0.0007) PB. The CD72 MFI was impressively higher on CD5+ than CD5- B cells in PB and SF of RA patients (P < 0.0001 and P < 0.005) and PB of SS patients (P < 0.005) and normal controls (P < 0.005). Our data suggest that, in association with CD4CD29, CD5 is involved in CD5+B/CD5+ B cell interactions in non-organ-specific autoimmune diseases.     

miR-199a靶向CSRP2对人风湿关节炎滑膜成纤维细胞的增殖、侵袭和炎症因子分泌的影响

目的:研究miR-199a对人风湿关节炎滑膜成纤维细胞MH7A增殖、侵袭和炎症因子分泌的影响及其机制.方法:将miR-199a mimics或/和pcDNA3.1-CSRP2转染至MH7A细胞,再以100 mg/L脂多糖(LPS)处理.用实时荧光定量PCR(RT-qPCR)检测细胞中miR-199a、富含半胱氨酸和甘氨...