Objective:To study the correlation of the expression of Eotaxin-3 and Foxm1 with the expression of p38MAPK/NF-κB and inflammatory factors in mucosa tissue of chronic sinusitis.Methods:57 patients with chronic sinusit...Objective:To study the correlation of the expression of Eotaxin-3 and Foxm1 with the expression of p38MAPK/NF-κB and inflammatory factors in mucosa tissue of chronic sinusitis.Methods:57 patients with chronic sinusitis and 38 patients with nasal septum deviation who received nasal endoscopic surgery in our hospital between March 2015 and August 2016 were selected and included in sinusitis group and control group respectively. Sinus mucosa tissues were collected to test the expression of Eotaxin-3, Foxm1, p38MAPK, NF-κB and inflammatory factors, and serum samples were collected to test the levels of inflammatory factors.Results:Eotaxin-3, Foxm1, p38MAPK and NF-κB protein expression in mucosa tissue of sinusitis group were significantly higher than those of control group, and the Eotaxin-3 and Foxm1 protein expression were positively correlated with p38MAPK and NF-κB protein expression;TGF-β1, IL-1β, IL-25, IL-33 and YKL-40 levels in nasal mucosa and serum of sinusitis group were significantly higher than those of control group, and TGF-β1, IL-1β, IL-25, IL-33 and YKL-40 levels in nasal mucosa and serum were positively correlated with p38MAPK and NF-κB protein expression.Conclusion:Eotaxin-3 and Foxm1 are expressed in mucosa tissue of chronic sinusitis, and can start the expression of inflammatory factors and induce the cascade amplification of inflammatory reaction through p38MAPK/ NF-κB signaling pathway.展开更多
Eosinophilic esophagitis(Eo E) is an allergy-mediated disease culminating in severe eosinophilic inflammation and dysfunction of the esophagus. This chronic disorder of the esophagus causes significant morbidity, poor...Eosinophilic esophagitis(Eo E) is an allergy-mediated disease culminating in severe eosinophilic inflammation and dysfunction of the esophagus. This chronic disorder of the esophagus causes significant morbidity, poor quality of life, and complications involving fibrosis and esophageal remodeling. Overlapping features between EoE and gastroesophageal reflux disease(GERD) pose great challenges to differentiating the two conditions, although the two disorders are not mutually exclusive. Recent findings suggest that the confounding condition proton pump inhibitor- responsive esophageal eosinophilia(PPI-REE) is likely a subset of EoE. Since PPIs have therapeutic properties that can benefit EoE, PPIs should be considered as a therapeutic option for Eo E rather than a diagnostic screen to differentiate GERD, PPIREE, and EoE. Other current treatments include dietary therapy, corticosteroids, and dilation. Immunomodulators and biologic agents might have therapeutic value, and larger trials are needed to assess efficacy and safety. Understanding the pathophysiology of EoE is critical to the development of novel therapeutics.展开更多
目的探讨转移相关蛋白2(MTA2)对前列腺癌预后的预测价值及在癌转移过程中的作用。方法收集空军军医大学第一附属医院2018年1月~2020年6月收治的50例前列腺癌患者的癌组织及配对癌旁组织样本用于免疫组织化学分析。根据MTA2蛋白的表达水...目的探讨转移相关蛋白2(MTA2)对前列腺癌预后的预测价值及在癌转移过程中的作用。方法收集空军军医大学第一附属医院2018年1月~2020年6月收治的50例前列腺癌患者的癌组织及配对癌旁组织样本用于免疫组织化学分析。根据MTA2蛋白的表达水平将样本分为两组,染色评分≥4为高表达组,<4为低表达组。对人前列腺癌细胞系(PC-3)转染shMTA2(MTA2-shRNA-pLKO.1)来沉默MTA2作为shMTA2组,转染Luc-shRNA-pLKO.1的细胞作为阴性对照组(shNC组),未转染的细胞作为空白对照组(control组)。通过MTT法检测细胞活力,Transwells实验进行体外迁移和侵袭分析。通过qRT-PCR或Western Blot检测细胞中MTA2、Eotaxin-1、CCR3、p-ERK1/2、t-ERK1/2和MMP-3的表达。结果前列腺癌组织中MTA2的染色评分显著高于癌旁组织(5.16±0.87 vs 2.34±0.39,t=9.221,P<0.001)。低表达组患者中出现淋巴结转移率为14.29%(2/14),高表达组患者中出现淋巴结转移率为52.78%(19/36),两组比较差异有统计学意义(χ^(2)=6.131,P=0.013)。与低表达组相比,高表达组患者的生存时间更长(χ^(2)=4.756,P=0.029)。与空白对照组相比,shMTA2组的细胞活力降低了56.87%(P<0.001),细胞迁移数量降低了65.80%(P<0.001),细胞侵袭数量降低了56.35%(P<0.001),Eotaxin-1、CCR3、p-ERK1/2和MMP-3的蛋白相对表达量依次降低了76.03%、69.12%、72.32%和54.67%(P<0.001)。结论前列腺癌组织中MTA2的表达水平升高且与患者的预后有关,沉默MTA2可降低前列腺癌细胞的迁移和侵袭能力,并抑制Eotaxin-CCR3-ERK1/2-MMP-3轴。展开更多
文摘Objective:To study the correlation of the expression of Eotaxin-3 and Foxm1 with the expression of p38MAPK/NF-κB and inflammatory factors in mucosa tissue of chronic sinusitis.Methods:57 patients with chronic sinusitis and 38 patients with nasal septum deviation who received nasal endoscopic surgery in our hospital between March 2015 and August 2016 were selected and included in sinusitis group and control group respectively. Sinus mucosa tissues were collected to test the expression of Eotaxin-3, Foxm1, p38MAPK, NF-κB and inflammatory factors, and serum samples were collected to test the levels of inflammatory factors.Results:Eotaxin-3, Foxm1, p38MAPK and NF-κB protein expression in mucosa tissue of sinusitis group were significantly higher than those of control group, and the Eotaxin-3 and Foxm1 protein expression were positively correlated with p38MAPK and NF-κB protein expression;TGF-β1, IL-1β, IL-25, IL-33 and YKL-40 levels in nasal mucosa and serum of sinusitis group were significantly higher than those of control group, and TGF-β1, IL-1β, IL-25, IL-33 and YKL-40 levels in nasal mucosa and serum were positively correlated with p38MAPK and NF-κB protein expression.Conclusion:Eotaxin-3 and Foxm1 are expressed in mucosa tissue of chronic sinusitis, and can start the expression of inflammatory factors and induce the cascade amplification of inflammatory reaction through p38MAPK/ NF-κB signaling pathway.
基金Supported by The National Institutes of Health(K08-DK099383 to Cheng E)NASPGHAN Foundation/Astra Zeneca Award(Cheng E)AGA Research Scholar Award(Cheng E)
文摘Eosinophilic esophagitis(Eo E) is an allergy-mediated disease culminating in severe eosinophilic inflammation and dysfunction of the esophagus. This chronic disorder of the esophagus causes significant morbidity, poor quality of life, and complications involving fibrosis and esophageal remodeling. Overlapping features between EoE and gastroesophageal reflux disease(GERD) pose great challenges to differentiating the two conditions, although the two disorders are not mutually exclusive. Recent findings suggest that the confounding condition proton pump inhibitor- responsive esophageal eosinophilia(PPI-REE) is likely a subset of EoE. Since PPIs have therapeutic properties that can benefit EoE, PPIs should be considered as a therapeutic option for Eo E rather than a diagnostic screen to differentiate GERD, PPIREE, and EoE. Other current treatments include dietary therapy, corticosteroids, and dilation. Immunomodulators and biologic agents might have therapeutic value, and larger trials are needed to assess efficacy and safety. Understanding the pathophysiology of EoE is critical to the development of novel therapeutics.
文摘目的探讨转移相关蛋白2(MTA2)对前列腺癌预后的预测价值及在癌转移过程中的作用。方法收集空军军医大学第一附属医院2018年1月~2020年6月收治的50例前列腺癌患者的癌组织及配对癌旁组织样本用于免疫组织化学分析。根据MTA2蛋白的表达水平将样本分为两组,染色评分≥4为高表达组,<4为低表达组。对人前列腺癌细胞系(PC-3)转染shMTA2(MTA2-shRNA-pLKO.1)来沉默MTA2作为shMTA2组,转染Luc-shRNA-pLKO.1的细胞作为阴性对照组(shNC组),未转染的细胞作为空白对照组(control组)。通过MTT法检测细胞活力,Transwells实验进行体外迁移和侵袭分析。通过qRT-PCR或Western Blot检测细胞中MTA2、Eotaxin-1、CCR3、p-ERK1/2、t-ERK1/2和MMP-3的表达。结果前列腺癌组织中MTA2的染色评分显著高于癌旁组织(5.16±0.87 vs 2.34±0.39,t=9.221,P<0.001)。低表达组患者中出现淋巴结转移率为14.29%(2/14),高表达组患者中出现淋巴结转移率为52.78%(19/36),两组比较差异有统计学意义(χ^(2)=6.131,P=0.013)。与低表达组相比,高表达组患者的生存时间更长(χ^(2)=4.756,P=0.029)。与空白对照组相比,shMTA2组的细胞活力降低了56.87%(P<0.001),细胞迁移数量降低了65.80%(P<0.001),细胞侵袭数量降低了56.35%(P<0.001),Eotaxin-1、CCR3、p-ERK1/2和MMP-3的蛋白相对表达量依次降低了76.03%、69.12%、72.32%和54.67%(P<0.001)。结论前列腺癌组织中MTA2的表达水平升高且与患者的预后有关,沉默MTA2可降低前列腺癌细胞的迁移和侵袭能力,并抑制Eotaxin-CCR3-ERK1/2-MMP-3轴。
文摘目的探讨细丝蛋白C(filamin C,FLNC)对前列腺癌细胞迁移和侵袭的影响。方法通过免疫组织化学分析了30例前列腺癌患者的癌组织及配对癌旁组织中FLNC的表达。根据FLNC蛋白的表达水平将30例前列腺癌患者分为FLNC低表达组(0~3分,n=9)和FLNC高表达组(4~12分,n=21),采用Kaplan-Meier法进行生存分析。对人前列腺癌细胞系(PC-3)转染抑制FLNC表达的小干扰RNA(siRNA-FLNC组)和阴性对照(siRNA-NC组),未转染的细胞作为对照组。通过MTT法检测细胞活力,Transwell实验进行迁移和侵袭分析。通过qRT-PCR或Western blot检测细胞中FLNC、Eotaxin-1、CCR3、p-ERK1/2、t-ERK1/2和MMP-3的表达。结果与癌旁组织相比,前列腺癌组织中FLNC的染色评分升高(1.43±0.86 vs 5.63±2.91,P<0.001)。FLNC低表达组和高表达组患者的TNM分期、淋巴结转移和生存时间差异有统计学意义(P<0.05)。与对照组相比,siRNA-FLNC组PC-3细胞中FLNC的mRNA和蛋白水平均降低(P<0.05),细胞活力降低(P<0.05),细胞迁移和侵袭数量降低(P<0.05)。与对照组相比,siRNA-FLNC组Eotaxin-1、CCR3、p-ERK1/2和MMP-3的蛋白相对表达量均降低(P<0.05),而t-ERK1/2的蛋白相对表达量无明显变化(P>0.05)。结论FLNC在前列腺癌组织中高表达并且与患者预后相关。沉默FLNC可能通过抑制Eotaxin-1-CCR3-ERK1/2-MMP-3通路降低前列腺癌细胞的迁移和侵袭能力。
