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小窝蛋白-1(Caveolin-1)是小窝标志性的蛋白,主要通过"脚手架"结构区域,参与负性调控多条信号通路,干预多种疾病进程.目前研究证实:特发性肺纤维化的肺组织中的Caveolin-1表达明显减低,而提高Caveolin-1水平抑制转化生长因子β_1/Smad、JNK、MEK/ERK、wnt/β-Catenin/Lef-1等信号转导通路因子的激活,可减少细胞外基质的合成和上皮细胞的异常修复,阻断肺纤维化进程.深入研究Caveolin-1参与肺纤维化的分子机制,有望为特发性肺纤维化提供新的分子治疗靶点. 相似文献
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目的 通过观察不同时间段机械通气大鼠肺组织中小窝蛋白-1(caveolin-1,cav-1)的表达水平,探讨cav-1在呼吸机所致肺损伤(VILI)发病中的作用.方法 雄性SD大鼠32只,随机分为对照组、通气0.5h组(H-VT0.5h组)、通气1h组(H-VT1h组)和通气2h组(H-VT2h组).采用免疫组织化学染色法测定各组大鼠肺组织cav-1的表达水平,测定其肺湿/干重(W/D)比值和支气管肺泡灌洗液(BALF)中总蛋白含量,并在光镜下观察各组大鼠肺组织的病理学改变.结果 ①肺组织cav-1表达结果显示,H-VT0.5h组和对照组均明显高于H-VT2h组和H-VT1h组(P值均<0.001),H-VT0.5h组明显高于对照组(P<0.001),H-VT1h组明显高于H-VT2h组(P<0.01).②肺组织W/D比值和BALF总蛋白含量测定结果显示,H-VT2h组和H-VT1h组均明显高于对照组和H-VT0.5h组(P值均<0.001),H-VT2h组明显高于H-VT1h组(P<0.001),H-VT0.5h组与对照组比较差异无统计学意义(P>0.05).③肺组织病理学结果显示,随着机械通气时间延长,大鼠肺组织损伤程度呈逐渐加重趋势.结论 肺组织cav-1在机械通气不同时间段表达水平明显不同,表现为先增高后降低.提示肺组织cav-1高表达对VILI起一定保护作用;大潮气量机械通气可通过抑制肺组织cav-1表达,诱发和加重肺组织损伤. 相似文献
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目的探讨Cav-1在肝癌细胞及其间质中的表达情况及临床意义。方法选取80例肝癌标本及其癌旁组织标本为研究对象,采用免疫组织化学法检测以上标本的Cav-1表达情况,并探讨Cav-1与肿瘤分化程度、周围器官侵犯、血管侵犯等病理参数的关系。结果 Cav-1在肝癌细胞中的表达显著高于癌旁组织,在肝癌间质的表达明显低于癌旁间质(P0.05)。Cav-1在肝癌实质中的表达与肝硬化、周围器官侵犯、血管侵犯、癌栓形成有关(P0.05)。Cav-1在肝癌间质中的表达与最大径,是否多发,是否有卫星、侵犯周围器官、血管侵犯、癌栓形成有关(P0.05)。结论 Cav-1在肝癌中的表达上调,在肝癌间质中的表达下降,其表达水平均与肝癌的侵袭性相关,可作为肝癌治疗的有效靶标。 相似文献
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<正>我国现有先天性心脏病(先心病)患者400余万,每年新增15~20万。左向右分流型先心病常常合并重度肺动脉高压(pulmonary arterial hypertension,PAH)和艾森蔓格综合征,部分患者在手术或介入治疗后PAH恢复正常 相似文献
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白介素32在气道炎症反应中的研究进展 总被引:1,自引:0,他引:1
在哮喘和慢性阻塞性肺疾病中,气道炎症反应始终贯穿疾病的发生、发展及转归.目前已发现有众多细胞及因子参与气道炎症反应,而白介素32作为一种新发现的细胞因子,很多文献证明其在炎症反应中有不可取代的作用.白介素32主要存在于自然杀伤细胞、T细胞、上皮细胞及外周血的单核细胞中,在自然免疫及特殊免疫中均有重要地位.在炎症反应中,白介素32可诱导某些因子的活性,如白介素类、肿瘤坏死因子α、核因子、促分裂原活化蛋白激酶及各种趋化因子,形成炎症级联式反应,造成气道局部的炎症,甚至引起全身性炎症反应.本文对白介素32在气道炎症中的作用作一综述. 相似文献
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目的 小凹(cavcolae)是细胞膜上的特异性凹陷,小凹蛋白(caveolin)是构成Caveolae的标志性蛋白,起到维持Caveolae结构的作用并参与胞吞和胞内运输作用、胆固醇运输、信号传导等过程.Caveolin-1富含于多种类型的细胞内,其中内皮细胞和平滑肌细胞是含量最丰富的细胞类型,对血管生成和平滑肌细胞增殖起重要作用. 相似文献
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目的 研究特发性肺纤维化(IPF)患者肺组织窖蛋白-1和细胞外基质表达的变化及其意义.方法 6例IPF患者的肺组织标本来自2005年1月至2008年12月南京大学医学院附属鼓楼医院呼吸科住院患者,其开胸肺活检组织病理诊断符合普通型间质性肺炎.6例肺癌患者行肺叶切除,取其远离病变的肺组织标本作为对照组.用RT-PCR、Western blot及免疫组织化学方法检测肺组织标本中的窖蛋白-1 mRNA和蛋白表达.Western blot检测肺组织标本的胶原-Ⅰ、α-平滑肌肌动蛋白(α-SMA)和Smads蛋白表达.结果 IPF患者肺组织窖蛋白-1的mRNA和蛋白表达(分别为0.05±0.02和0.16±0.05)明显低于对照组(分别为0.66±0.19和0.81±0.11),差异有统计学意义(F值分别为8.465和353.836,均P<0.05).IPF患者肺组织的胶原-Ⅰ (0.85±0.11)和α-SMA蛋白(0.78±0.08)表达明显高于对照组(分别为0.16±0.04和0.14±0.05),差异有统计学意义(F值分别为485.09、410.027,均P<0.05).IPF患者肺组织的p-Smad2蛋白(0.78±0.08)和p-Smad3蛋白(0.86±0.07)表达明显高于对照组(分别为0.17±0.04和0.14±0.04),差异有统计学意义(F值分别为521.97和530.48,均P<0.05);而Smad7蛋白表达(0.22±0.05)明显低于对照组(0.78±0.08),差异有统计学意义(F=414.84,P<0.05).结论 IPF患者肺组织窖蛋白-1表达下调与特发性肺纤维化的发生和发展有关. 相似文献
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Chronic NOS inhibition prevents adverse lung remodeling and pulmonary arterial hypertension in caveolin-1 knockout mice 总被引:1,自引:0,他引:1
Wunderlich C Schmeisser A Heerwagen C Ebner B Schober K Braun-Dullaeus RC Schwencke C Kasper M Morawietz H Strasser RH 《Pulmonary pharmacology & therapeutics》2008,21(3):507-515
Recently generated caveolin-1 deficient mice (cav-1 ko) suffer from severe lung fibrosis with marked pulmonary hypertension and arterial hypoxemia and may therefore serve as an useful animal model of this devastating human disorder. Accumulating evidence strongly supports the negative regulatory influence of caveolin-1 on endothelial nitric oxide synthase resulting in a constitutive hyperactivation of the nitric oxide (NO) pathway in cav-1 ko. We therefore hypothesized that a disturbed NO signaling is implicated in the evolution of the adverse lung phenotype of cav-1 ko. For this purpose, cav-1 ko of 2 months age were compared with knockout counterparts experiencing 2-month postnatal NO synthase inhibition by NG-nitro-l-arginine methyl ester (L-NAME) treatment. Chronic l-NAME administration prevented adverse lung remodeling in cav-1 ko. Furthermore, l-NAME donation led to a normalized oxygen saturation (91.5+/-1.8% vs. 98.5+/-2.3%, P<0.01, n=10-12), a marked decrease in right ventricular hypertrophy (LV/RV ratio: 4.0+/-0.3 vs. 2.7+/-0.3, P<0.01, n=10-12) and reductions of the elevated pulmonary artery pressure (40.2+/-3.1 mmHg vs. 26.3+/-4.6 mmHg, P<0.01, n=6). Collectively, these improvements resulted in an enhanced exercise capacity of l-NAME-treated cav-1 ko. Finally, we found evidence for enhanced oxidative stress in untreated cav-1 ko which was substantially reduced by chronic l-NAME administration to cav-1 ko. In view of these data, we speculate that a perturbation of NO signaling, together with enhanced O2(-) production originating from NO synthases, may play a pivotal role in the pathogenesis of the adverse pulmonary phenotype seen in cav-1 ko. 相似文献
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Novel mechanism for sudden infant death syndrome: Persistent late sodium current secondary to mutations in caveolin-3 总被引:3,自引:0,他引:3
Lisa B. Cronk BA Bin Ye PhD Toshihiko Kaku MD PhD David J. Tester BS Matteo Vatta PhD Jonathan C. Makielski MD Michael J. Ackerman MD PhD 《Heart rhythm》2007,4(2):161-166
BACKGROUND: Sudden infant death syndrome (SIDS) is one of the leading causes of death during the first year of life. Long QT syndrome (LQTS)-associated mutations may be responsible for 5% to 10% of SIDS cases. We recently established CAV3-encoded caveolin-3 as a novel LQTS-associated gene with mutations producing a gain-of-function, LQT3-like molecular/cellular phenotype. OBJECTIVE: The purpose of this study was to determine the prevalence and functional properties of CAV3 mutations in SIDS. METHODS: Using polymerase chain reaction, denaturing high-performance liquid chromatography, and DNA sequencing, postmortem genetic testing of CAV3 was performed on genomic DNA isolated from frozen necropsy tissue on a population-based cohort of unrelated cases of SIDS (N = 134, 57 females, average age = 2.7 months). CAV3 mutations were engineered using site-directed mutagenesis and heterologously expressed in HEK293 cell lines stably expressing the SCN5A-encoded cardiac sodium channel. RESULTS: Overall, three distinct CAV3 mutations (V14L, T78M, and L79R) were identified in three of 50 black infants (6-month-old male, 2-month-old female, and 8 month-old female), whereas no mutations were detected in 83 white infants (P <.05). CAV3 mutations were more likely in decedents 6 months or older (2/12) than in infants who died before 6 months (1/124, P = .02). Voltage clamp studies showed that all three CAV3 mutations caused a significant fivefold increase in late sodium current compared with controls. CONCLUSION: This study provides the first molecular and functional evidence implicating CAV3 as a pathogenic basis of SIDS. The LQT3-like phenotype of increased late sodium current supports an arrhythmogenic mechanism for some cases of SIDS. 相似文献
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《中华结核和呼吸杂志》2009,32(11)
目的 利用量子点免疫荧光标记技术检测窖蛋白-1(Cav-1)在人肺癌组织芯片中的表达,探讨Cav-1与细胞外基质金属蛋白酶诱导物(CD_(147)/EMMPRIN)及基质金属蛋白酶-2(MMP-2)表达的关系.方法 利用量子点免疫荧光组织化学结合组织芯片技术检测Cav-l、CD_(147)和MMP-2在70例肺癌和5例非癌变肺组织中的表达.结果 肺癌组Cav-1平均荧光强度为55 ±23,低于对照组的80±4(t=2.461,P=0.016);Cav-1表达与肺癌患者的性别、年龄和组织学类型无关,但与TNM分期(t=2.466,P=0.016)和淋巴结转移(t=2.972,P=0.004)均显著相关;Cav-1与CD_(147)表达呈显著负相关(r=-0.331,P=0.005),与MMP-2表达无关.结论 量子点免疫荧光组织化学技术可精确定量检测肺癌组织芯片上的不同蛋白表达.Cav-1与肺癌的发生密切相关,其高表达可促进肺癌细胞的侵袭转移,其机制可能与调节CD_(147)而不是MMP-2的活性有关. 相似文献