Serum of cytomegalovirus-infected mice induces monocyte chemoattractant protein-1 expression by endothelial cells

Inflammation plays a central role in atherogenesis. It was hypothesized that infection of apolipoprotein E-deficient mice with murine cytomegalovirus (MCMV) increases serum levels of proinflammatory cytokines, which may induce "proatherosclerotic" changes in endothelial cells (ECs). Serum samples were collected from uninfected and infected mice. ELISA was used to determine cytokine serum levels and monocyte chemoattractant protein-1 (MCP-1) levels in the supernatant of mouse ECs incubated with serum-containing medium. Serum samples from infected mice induced MCP-1 expression by ECs. These serum samples contain interferon (IFN)-gamma, whereas IFN-gamma was undetectable in serum samples from uninfected mice. Preincubating infected mouse serum with anti-IFN-gamma monoclonal antibody significantly decreased serum-induced EC expression of MCP-1. Thus, MCMV infection increases IFN-gamma serum levels, such serum can induce MCP-1 in ECs, and the serum-induced MCP-1 expression is due, at least in part, to IFN-gamma. If these changes in EC function also occur in vivo in response to infection, they could exacerbate atherogenesis.     

结直肠癌趋化因子单核细胞超化蛋白-1的表达

目的：通过检测结直肠癌组织中单核细胞超化蛋白－1（MPC－1）的表达情况，研究MCP－1的表达与结直肠癌生物学行为的关系。方法：采用RT－PCR方法，检测临床收集的新鲜结肠癌组织标本中MCP－1mRNA的表达；采用免疫组化方法，检测结直肠癌组织中MCP－1蛋白的表达，结果：12例结直肠癌组织均可出现MCP－1mRNA的表达，40例结直肠癌组织MCP－1蛋白表达的阳性率为90％，结直肠癌组织MCP－1蛋白的表达与结直肠癌的转移及Dukes分期有关，表达强者，转移发生率低，Dukes分期早，结论：结直肠组织中MCP－1的表达能影响结直肠癌的生物学行为。     

Doxycycline decreases monocyte chemoattractant protein-1 in human lung epithelial cells

Certain antibiotics possess anti-inflammatory properties and could potentially be used to treat inflammatory lung diseases associated with an influx of monocytes such as panbronchiolitis, asthma, cystic fibrosis, and bronchitis. Doxycycline is reported to possess anti-inflammatory effects. Monocyte chemoattractant protein-1 (MCP-1) is a major inflammatory cytokine and a powerful chemoattractant for monocytes. The authors hypothesized that doxycycline exerts its anti-inflammatory effects, in part, by reducing MCP-1 production. To test this hypothesis, A549 human lung epithelial cells were stimulated with cytomix in the presence or absence of doxycycline. In stimulated cells doxycycline decreased MCP-1 production by 95% and in monocyte chemotaxis assays migration decreased by 55%. However, doxycycline did decrease expression of MCP-1 mRNA and did not effect its stability. These data demonstrate that doxycycline modulates MCP-1 production and suggest that doxycycline may provide a new anti-inflammatory therapy for chronic lung diseases.     

Induction of monocyte chemoattractant protein-1 expression by angiotensin II in the pancreatic islets and beta-cells

Angiotensin II (AngII), the principal hormone of the renin-angiotensin system, is actively generated in the pancreas and has been suggested as a key mediator of inflammation. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that plays an important role in the recruitment of mononuclear cells into the pancreatic islets. In this study, we investigated the potential molecular basis for the role of AngII in islet inflammation through studying its effect on MCP-1. AngII significantly increased the expression of MCP-1 mRNA and protein in the RINm5F beta-cell line and activated MCP-1 promoter. AngII-MCP-1 mRNA induction was inhibited by an AngII type 1 receptor antagonist but was unchanged by an AngII type 2 receptor antagonist. AngII-MCP-1 induction was inhibited by the tyrosine kinase inhibitor genistein, suggesting a MAPK signaling mechanism. AngII activated the phosphorylation of ERK1/2 but not p38 or c-Jun NH(2)-terminal MAPKs. Inhibition of ERK1/2 activation reduced the AngII-induced MCP-1 synthesis. In nonobese diabetic mice pancreata, the temporal pattern of angiotensin-converting enzyme expression correlated well with progression of insulitis and beta-cell destruction. Immunostaining of pancreatic serial sections show colocalization of angiotensin-converting enzyme with MCP-1 in beta-cells in the islets. In freshly isolated islets from normoglycemic mice, AngII alone and in combination with IL-1beta elicited an inflammatory response by stimulation of MCP-1. Our data suggest a positive autocrine/paracrine action for the local pancreatic AngII-generating system during insulitis and provide the first insight into an AngII-initiated signal transduction pathway that regulates MCP-1 as a possible inflammatory mechanism in the islets.     

玉葵清对糖基化终产物诱导的人肾系膜细胞趋化因子表达的影响

目的 探讨玉葵清对糖基化终产物（AGEs）诱导的人肾系膜细胞（HRMC）趋化因子表达及其趋化效应的影响. 方法 糖基化牛血清白蛋白（AGE-BSA）和玉葵清干预HRMC. 结果 AGE-BSA组较BSA组HRMC趋化单核细胞数增加,单核细胞趋化蛋白-1（MCP-1）、Fractalkine（FKN）中和抗体组HRMC趋化单核细胞数较AGE-BSA组减少;玉葵清组MCP-1、Fractalkine基因表达、上清中的蛋白含量和趋化单核细胞较BSA组降低（P＜0.05）. 结论 玉葵清减弱AGE-BSA诱导的HRMC趋化因子表达及其趋化效应,可能改善DN肾脏炎症反应.     

醛固酮对大鼠肾小球系膜细胞单核细胞趋化蛋白1表达和合成的影响

目的 探讨醛固酮对大鼠肾小球系膜细胞表达和合成单核细胞趋化蛋白1(MCP-1)的影响. 方法 采用高糖(17.5mmol/L,Con组)、高糖+不同浓度醛固酮、高糖+螺内酯+醛固酮培养大鼠系膜细胞.24h后检测各组MCP-1 mRNA表达和MCP-1蛋白的浓度. 结果 与Con组比较,10-5、10-7和10-9mol/L醛固酮组系膜细胞上清中MCP-1水平明显增高.RT-PCR结果显示醛固酮可显著上调MCP-1 mRNA的表达(P<0.01),而螺内酯可部分抑制醛固酮诱导的MCP-1高表达. 结论 醛固酮可上调大鼠肾小球系膜细胞MCP-1 mRNA的表达和蛋白质合成.     

单核细胞趋化蛋白-1在系统性硬化症患者中的表达

目的 探讨单核细胞趋化蛋白-1（MCP-1）在系统性硬化症（SSc）的相关性。方法 采用酶联免疫吸附试验（ELISA）方法检测27例SSc患者血浆MCP-1水平，并与21名年龄和性别相匹配的健康志愿者血浆中浓度对照，同时采用反转录聚合酶链反应（RT-PCR）和免疫组织化学染色方法检测MCP-1mRNA和蛋白质在5例SSc患者和3名健康志愿者皮肤成纤维细胞中的表达。结果 血浆MCP-1水平SSc组为（787±393）pg／ml，明显高于健康志愿者组的（426±266）pg/ml（P〈0．05）。对SSc组的进一步分析显示，11例弥漫型SSc患者血浆MCP-1水平为（896±347）pg／ml，高于16例局限型SSc患者的（714±332）pg/ml（P〈0．05）；18例并发有肺间质纤维化的SSc患者血浆MCP-1水平（844±327）pg／ml，也高于9例无肺间质纤维化的SSc患者的（676±314）pg／ml（P〈0．05）。RT-PCR和免疫组织化学染色的结果显示，5例分离于SSc病变皮肤、在体外培养的成纤维细胞有MCP-1的mRNA和蛋白质分子表达，而3名取自健康志愿者皮肤的成纤维细胞则无表达。结论 SSc患者血浆MCP-1水平显著升高，而且与皮肤受累程度和肺间质纤维化有一定的关系。RT-PCR和免疫组织化学染色结果表明，SSc患者病变皮肤组织表达MCP-1增高，提示MCP-1在SSc的病程中起重要作用。     

单核细胞趋化蛋白-1与糖尿病肾病

糖尿病肾病(DN)是终末肾功能衰竭的主要原因,主要的病理改变是肾小球肥大、细胞外基质积聚以及肾小球硬化.多种机制参与了DN的发生、发展,其中肾脏被炎性反应细胞如单核/巨噬细胞浸润是DN的标志之一.单核细胞趋化蛋白-1(MCP-1)是一种对单核细胞具有特异趋化功能的细胞因子,参与单核/巨噬细胞的浸润,在DN的发生、发展中起重要作用.