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Vimentin

Vimentin的相关文献在1991年到2023年内共计177篇,主要集中在肿瘤学、基础医学、外科学 等领域,其中期刊论文166篇、专利文献11篇;相关期刊120种,包括现代生物医学进展、中国实验诊断学、现代消化及介入诊疗等; Vimentin的相关文献由777位作者贡献,包括刘芳、夏红、苏琦等。

Vimentin—发文量

期刊论文>

论文:166 占比:93.79%

专利文献>

论文:11 占比:6.21%

总计:177篇

Vimentin—发文趋势图

Vimentin

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  • 刘芳
  • 夏红
  • 苏琦
  • 凌晖
  • 曾希
  • 苏坚
  • 苏波
  • 万源
  • 刘刚
  • 刘志明
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    • Kang-Zhen Chen; Shu-Xian Liu; Yan-Wei Li; Tao He; Jie Zhao; Tao Wang; Xian-Xiu Qiu; Hong-Fu Wu
    • 摘要: Vimentin is a major type Ⅲ intermediate filament protein that plays important roles in several basic cellular functions including cell migration, proliferation, and division. Although vimentin is a cytoplasmic protein, it also exists in the extracellular matrix and at the cell surface. Previous studies have shown that vimentin may exert multiple physiological effects in different nervous system injuries and diseases. For example, the studies of vimentin in spinal cord injury and stroke mainly focus on the formation of reactive astrocytes. Reduced glial scar, increased axonal regeneration, and improved motor function have been noted after spinal cord injury in vimentin and glial fibrillary acidic protein knockout(GFAPVIM) mice. However, attenuated glial scar formation in post-stroke in GFAP–/– VIM–/– mice resulted in abnormal neuronal network restoration and worse neurological recovery. These opposite results have been attributed to the multiple roles of glial scar in different temporal and spatial conditions. In addition, extracellular vimentin may be a neurotrophic factor that promotes axonal extension by interaction with the insulin-like growth factor 1 receptor. In the pathogenesis of bacterial meningitis, cell surface vimentin is a meningitis facilitator, acting as a receptor of multiple pathogenic bacteria, including E. coli K1, Listeria monocytogenes, and group B streptococcus. Compared with wild type mice, VIMmice are less susceptible to bacterial infection and exhibit a reduced inflammatory response, suggesting that vimentin is necessary to induce the pathogenesis of meningitis. Recently published literature showed that vimentin serves as a double-edged sword in the nervous system, regulating axonal regrowth, myelination, apoptosis, and neuroinflammation. This review aims to provide an overview of vimentin in spinal cord injury, stroke, bacterial meningitis, gliomas, and peripheral nerve injury and to discuss the potential therapeutic methods involving vimentin manipulation in improving axonal regeneration, alleviating infection, inhibiting brain tumor progression, and enhancing nerve myelination.
    • 徐胜昔; 李森; 石颖芳; 王恒丹; 李梦琴; 汪志春
    • 摘要: 目的探讨早期乳腺癌非前哨淋巴结转移的独立风险因素。方法收集111例早期乳腺癌患者的临床病理资料,临床腋窝表现为阴性,成功行前哨淋巴结活检,显示为阳性,随后行同侧腋窝淋巴结清扫,应用统计学软件对相关因素进行分析。将单因素分析有统计学显著意义的因素纳入logistic多因素回归分析,找出非前哨淋巴结转移的独立风险因素。结果在单因素分析中,患者年龄、原发肿瘤大小、与淋巴管血管侵犯状况、Ki-67状态、SLN转移阳性数(SLN+)、SLN转移阴性数(SLN-)、SLN转移阳性数占SLN总数的比例(SLN+/SLN)、纤维连接蛋白1(FN1)表达以及波形蛋白(Vimentin)表达等因素在非前哨淋巴结阳性组与阴性组间有统计学差异,对以上因素采用二元logistic回归分析,结果显示原发肿瘤大小,纤维连接蛋白1(FN1)表达水平以及波形蛋白(Vimentin)表达水平,两组具有统计学上差异(P<0.05)。结论原发肿瘤大小,FN1(-)以及Vimentin(+)是早期乳腺癌非前哨淋巴结转移的独立风险因素。
    • 鞠玮; 史圆圆; 黄育萌; 许建辉; 严志新; 杨细虎
    • 摘要: 目的 探讨腮腺内面神经鞘瘤的临床特点及病理特征。方法 收集2015—2020年江苏大学附属医院口腔颌面外科收治的5例腮腺内面神经鞘瘤病例,分析患者的临床资料、影像资料、病理资料、术前诊断、治疗方式及术后神经损伤情况等。结果 5例患者均为男性,年龄33~70岁。临床表现仅为境界清楚的无痛性腮腺区肿物,均不伴面神经瘫痪等症状。2例术前诊断为混合瘤,3例术前诊断为腺淋巴瘤。治疗方式为肿瘤合并神经切除后神经端端吻合术。术后随访4例患者面神经功能基本正常,仅一例患者存在H-BⅡ级面神经功能障碍症状,随访10~72个月未见复发病例及恶变。镜下肿瘤细胞呈长梭形,呈编织状排列。免疫组化示肿瘤细胞S-100蛋白在5例患者的细胞核和细胞质中呈弥漫性强阳性表达,Vimentin在5例患者胞质中均呈强阳性表达,Sox10在4例患者胞核中呈阳性表达,3例患者局灶表达CK7,细胞增殖能力标记物Ki-67阳性指数均小于3%,AE1、EMA、P63、SMA在全部病例中均呈阴性表达。结论 腮腺内面神经鞘瘤的临床表现及辅助检查均无特异性,术前确诊较为困难,需要依赖病理诊断,S-100、Vimentin可辅助诊断腮腺内面神经鞘瘤。
    • 李林; 付盈盈; 司应明
    • 摘要: 目的:研究积雪草苷对人鼻咽癌CNE-2细胞生长、凋亡及凋亡通路的影响。方法:体外培养CNE-2细胞,将不同浓度的积雪草苷作用于CNE-2细胞,MTT和CCK-8法检测积雪草苷对细胞生长的影响;流式细胞术检测对细胞凋亡的影响;Western blotting检测Vimentin、NLRP3、Bcl-2和Caspase-3表达;ELISA法检测TNF-α和IL-1β含量。结果:MTT和CCK-8结果显示,积雪草苷可浓度依赖性地抑制CNE-2细胞的生长;流式细胞仪检测结果显示,积雪草苷可浓度依赖性地促进CNE-2细胞凋亡;Western blotting结果显示,积雪草苷促进Caspase-3蛋白的表达,抑制Vimentin、NLRP3和Bcl-2的表达;ELISA法结果显示,积雪草苷可浓度依赖性地降低TNF-α和IL-1β含量。结论:积雪草苷可显著促进人鼻咽癌细胞株CNE-2细胞凋亡,其机制可能与下调Vimentin,NLRP3蛋白的表达来实现的。
    • Wanyue Han; Qingshan Li; Qing Zhang; Fan Xu
    • 摘要: Breast cancer stem cells (BCSCs) are a small subpopulation of cancer cells having the ability of self-renewing and multi-lineage differentiation, which have also been termed as “tumor-initiating cells”. And in recent years, the role of epithelial mesenchymal transition (EMT) in malignant tumors has been valued. This paper will briefly review and discuss the relationship between BCSCs and EMT.
    • Chao Li; Yu-Qing Ma
    • 摘要: BACKGROUND Sex determining region Y-box 2(SOX2) can promote squamous cell carcinoma(SSC) because it regulates the migration and invasion of several different types of squamous carcinoma cells.However,few studies have examined the prognostic value of SOX2 and its effect on the epithelial-mesenchymal transition(EMT) in esophageal SSC(ESCC),a cancer characterized by high invasion and rapid metastasis.AIM To verify the relationship of SOX2 and the EMT in ESCC and determine the prognostic value and significance of SOX2 and protein markers of the EMT in ESCC.METHODS One hundred and eighty-five postsurgical ESCC patients were retrospectively examined.Immunohistochemistry was used to detect SOX2,E-cadherin,and vimentin in ESCC tissues.The chi-square test was used to determine the relationships of the expression of these proteins with clinical data.Kaplan-Meier survival curves were used to evaluate factors associated with overall survival(OS).RESULTS SOX2 and vimentin had high expression in ESCC tissues and correlated with the depth of local carcinoma invasion.SOX2 expression had positive correlations with tumor size,vimentin expression,and the EMT,and a negative correlation with Ecadherin expression.Expression of SOX2 and vimentin had negative correlations with OS.SOX2 expression was an independent prognostic risk factor for poor OS in patients with ESCC.CONCLUSION SOX2 expression was an independent risk factor for OS in patients with ESCC and its expression had a positive correlation with the expression of vimentin,a classic marker of the EMT.SOX2 promoted the migration and invasion of ESCC,and this may related to its effect on vimentin in promoting the EMT.
    • 郝琳; 康娟; 宋英
    • 摘要: 目的研究GOLPH3与非小细胞肺癌上皮间质转化的相关性。方法选取72例非小细胞肺癌患者作为研究对象。对比患者肺癌组织和癌旁正常组织中高尔基磷酸化蛋白3(GOLPH3)、上皮间之转化标志物E-钙黏素(E-cadherin)以及波形蛋白(vimentin)水平;对比不同临床特征(病理类型、分化程度、淋巴结转移情况)GOLPH3表达情况,同时分析GOLPH3与E-cadherin和vimentin表达相关性。结果肺癌组织GOLPH3和vimentin阳性率均显著高于癌旁正常组织,E-cadherin阳性率显著低于癌旁正常组织(P<0.05);不同分化程度、是否存在淋巴结转移以及不同TNM分期患者GOLPH3、E-cadherin和vimentin阳性表达率差异具有统计学意义(P<0.05);经过相关性分析得出:GOLPH3阳性表达率与E-cadherin表达呈负相关,与vimentin呈正相关(P<0.05)。结论GOLPH3与非小细胞肺癌患者E-cadherin表达呈负相关,与vimentin呈正相关,与患者上皮间质转化存在明显的相关性。
    • 赵媛; 李冰; 陶月佳; 黄允宁; 徐远义
    • 摘要: 目的研究微小RNA(miR)-34c-5p在胃癌组织中的表达及调控胃癌细胞侵袭和迁移机制。方法利用实时荧光定量聚合酶链式反应(RT-qPCR)检测人胃癌组织及胃癌细胞中miR-34c-5p mRNA表达;在人胃癌细胞中构建miR-34c-5p过表达模型,倒置荧光显微镜观察慢病毒转染情况,RT-qPCR验证转染效率。利用划痕实验、Transwell实验检测过表达miR-34c-5p对胃癌细胞侵袭和迁移的影响;通过Western blot检测各组胃癌细胞中MAP2K1、E-钙黏蛋白(E-cadherin)及波形蛋白(Vimentin)的表达情况。双萤光素酶报告基因检测MAP2K1是否是miR-34c-5p的靶基因。结果miR-34c-5p mRNA在10例人胃癌组织中的表达明显低于癌旁组织(P<0.05);miR-34c-5p mRNA在胃癌HGC-27细胞中的表达明显低于正常胃黏膜GES-1细胞(P<0.01);与空白对照组、miR-34c-5p-NC组比较,miR-34c-5p-mimics组miR-34c-5p mRNA表达水平明显升高(P<0.05);划痕实验及Transwell实验结果表明,过表达miR-34c-5p明显抑制了胃癌细胞的迁移和侵袭能力(P<0.05,P<0.01);Western blot检测结果表明,过表达miR-34c-5p后胃癌HGC-27细胞中MAP2K1、Vimentin蛋白表达水平明显降低,E-cadherin蛋白表达水平明显升高(P<0.05);此外,与mimic-NC+miR-34c-5p-mimics组相比,转染pmiR-MAP2K1-WT质粒细胞的萤光素酶活性降低(P<0.01),而转染pmiR-MAP2K1-Mut质粒的萤光素酶活性无改变。结论miR-34c-5p在胃癌组织和胃癌细胞中低表达,可能通过靶向调控MAP2K1表达抑制胃癌细胞侵袭和迁移。
    • 徐夏; 江海; 陈豫民; 王琰
    • 摘要: 目的:探究STAT3、E-cadherin、Vimentin在食管鳞癌上皮间质转化过程中产生的影响.方法:采用RT-qPCR方法检测50例食管鳞癌组织及癌旁正常组织中STAT3、E-cadherin、Vimentin的mRNA水平表达,分析癌组织、癌旁正常组织相对表达量与临床病理特征间的关系;随机抽取4例食管鳞癌患者组织标本,采用Western blot方法检测STAT3、E-cadherin、Vimentin蛋白水平表达.采用RT-qPCR及Western blot方法检测三种食管鳞癌细胞株中STAT3、E-cadherin、Vimentin表达,筛选出1株高表达STAT3的菌株,用STAT3的小干扰RNA转染.对照组转染双链无义RNA,转染成功后进行细胞划痕实验及Transwell细胞侵袭实验.结果:50例食管鳞癌组织中STAT3、E-cadherin、Vimentin相对表达量分别为(1.81±0.62)、(0.68±0.23)、(1.48±0.56);癌旁正常组织为(0.54±0.23)、(2.03±0.64)、(0.61±0.21).食管鳞癌中STAT3、Vimentin在mRNA水平高表达及E-cadherin低表达,在浸润深度、淋巴结转移方面比较,差异均有统计学意义(P<0.05).检测随机4例食管鳞癌患者组织标本蛋白水平表达,癌组织中STAT3、Vimentin均比癌旁正常组织高(P<0.05),而癌组织中E-cadherin比癌旁正常组织低(P<0.05).STAT3小干扰RNA转染高表达STAT3的细胞株EC109后,STAT3表达在mRNA水平较对照组下调,E-cadherin表达较对照组相对上调;Vimentin表达较对照组相对下调,差异均有统计学意义(P<0.05);在蛋白水平,转染STAT3小干扰RNA组较对照双链无义RNA组成功抑制STAT3蛋白表达(P<0.05),E-cadherin蛋白表达相对上调(P<0.05),Vimentin蛋白表达相对下调(P<0.05).细胞划痕结果显示,转染STAT3小干扰RNA组EC109的36、72 h迁移率均低于对照双链无义RNA组,差异均有统计学意义(P<0.05);侵袭实验结果显示,转染STAT3小干扰RNA组的EC109穿入小室膜底部的细胞总数较对照双链无义RNA组减少,差异有统计学意义(P<0.05),下调STAT3表达后食管鳞癌细胞株EC109迁移、侵袭能力减弱.结论:STAT3可能通过调控E-cadherin、Vimentin影响食管鳞癌上皮间质转化,从而影响肿瘤迁移与侵袭.
    • 张晨宇; 谢甦; 谢青; 胡雅清; 朱蔓荆; 郑丽
    • 摘要: 目的 探究薯蓣丸联合环磷酰胺对乳腺癌小鼠上皮细胞4T1体内间-充质转换(EMT)的影响.方法 将24只6周龄BALB/c小鼠随机分为模型组、环磷酰胺组、薯蓣丸联合环磷酰胺组,每组8只,注射4T1细胞悬液复制荷瘤模型.其间每3d测量小鼠肿瘤体积,绘制肿瘤生长曲线;给药21 d后,称定小鼠瘤重,计算抑瘤率;Western blot检测小鼠瘤组织E-cadherin、Vimentin、Akt及p-Akt蛋白表达;RT-PCR检测E-cadherin、Vimentin mRNA表达.结果 给药6d后,与模型组相比,环磷酰胺组、薯蓣丸联合环磷酰胺组肿瘤体积减小,生长速率减缓(P<0.05);给药15 d后,与环磷酰胺组相比,薯蓣丸联合环磷酰胺组肿瘤体积较小,生长速率均减缓(P<0.05),环磷酰胺组、薯蓣丸联合环磷酰胺组抑瘤率分别为33.6%、46.75%.与模型组比较,环磷酰胺组、薯蓣丸联合环磷酰胺组瘤组织Vimentin蛋白及mRNA表达降低(P<0.05),E-cadherin蛋白及mRNA表达增加(P<0.05),p-Akt/Akt蛋白表达降低(P<0.05),其中薯蓣丸联合环磷酰胺组较环磷酰胺组以上指标变化更为明显(P<0.05).结论 薯蓣丸联合环磷酰胺对肿瘤的生长有一定的抑制作用,能降低乳腺癌小鼠瘤组织Vimentin蛋白及mRNA、p-Akt/Akt蛋白表达,并提高E-cadherin蛋白及mRNA表达,可以抑制乳腺癌小鼠上皮4T1细胞EMT.
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