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光动力处理的角质形成细胞衍生的细胞因子旁分泌诱导成纤维细胞内基质金属蛋白酶的合成
研究背景和目的新近的研究发现,5-氨基酮戊酸(5-aminolevulinic acid,ALA)介导的光动力学疗法(photodynamic therapy,PDT)能够直接影响成纤维细胞所生成具有胶原降解作用的基质金属蛋白酶(matrix metalloproteinase,MMP)-1和MMP-3的水平,并认为这与ALA-PDT治疗局限性硬皮病的抗硬化效应有关.
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基质金属蛋白酶及其抑制剂在结直肠癌中的作用研究进展
结直肠癌是常见的消化道恶性肿瘤之一。在世界范围内其发病率和死亡率分别位于恶性肿瘤的第3位和第4位[1]。结直肠癌的发病是环境、饮食、生活习惯及遗传等多因素协同作用的结果,目前对结直肠癌发病的具体机制还不明确。结直肠癌发病有关的危险因素有吸烟、缺乏身体锻炼、肥胖、红肉和肉制品食用过多以及酒精摄入过多等[2]。在结直肠癌患者的治疗中影响生存和预后的重要因素是肿瘤的侵袭和转移。基质金属蛋白酶(matrix metalloproteinase,MMPs)是降解细胞外基质的重要酶类,几乎能降解细胞外基质的所有成分[3]。MMPs能通过破坏基质的降解平衡来促进肿瘤细胞突破基底膜和细胞外基质构成的组织屏障,从而使肿瘤细胞更易于向周围组织侵袭和转移。基质金属蛋白酶组织抑制剂(tissue inhibitor of matrix metalloproteinases,TIMPs)是MMPs的天然抑制物。MMPs与TIMPs之间的平衡关系在肿瘤转移中有重要作用,本文就MMPs及TIMPs在结直肠癌中的作用研究进展作一综述。
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基质金属蛋白酶及其抑制因子在脑外伤大鼠脑水肿区表达的研究
1目的脑外伤后继发脑水肿是血管源性脑水肿,血管基底膜损坏可能在血管源性脑水肿中起重要作用.明胶酶A(gelatinase A,又称MMP-2)和明胶酶B(celatinase B,又称MMP-9)可降解血管基底膜的主要成分--Ⅳ型胶原.我们用逆转录定量PCR方法研究大鼠脑外伤后水肿区脑组织基质金属蛋白酶(tissue matrix metalloproteinases,MMPs)及其抑制因子(tissue inhibiter of matrix metalloproteinases,TIMPs)基因表达情况,探讨其与脑水肿发生机制的关系.
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基质金属蛋白酶及其抑制物在膀胱癌中的表达及意义
为探讨基质金属蛋白酶(matrix metalloproteinases, MMPs)及其基质蛋白酶抑制物(tissue inhibitor of matrix metalloproteinases, TIMPs)在膀胱移行细胞癌(TCCB)中的表达及意义,我们对51例TCCB及10例正常膀胱组基质金属蛋白酶及其抑制物在膀胱癌中的表达进行了检测.
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基质金属蛋白酶及其抑制物蛋白表达与肾癌预后的关系
肿瘤从原位的增殖性肿瘤到侵袭性转移的演化过程中,肿瘤必须具备降解细胞外基质(extracell matrix,ECM)的能力.基质金属蛋白酶(matrix metalloproteinases,MMPs)具有降解ECM的能力,从而促进癌细胞对周围组织的浸润.MMPs的活性受组织基质金属蛋白酶抑制物(tissue inhibitor of matrix metalloproteinases,TIMPs)的影响.我们应用免疫组化技术检测MMP2、MMP9和TIMP1在肾癌中的表达,探讨与其病理分级、分期和预后的关系.
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明胶酶及其组织抑制物基因在卵巢上皮性肿瘤组织中的表达及意义
卵巢上皮性癌(卵巢癌)在就诊时多已发生转移.目前的研究认为,明胶酶A(matrix metalloproteinase-2,MMP-2)和明胶酶B(matrix metalloproteinase-9,MMP-9)与肿瘤的侵袭、转移密切相关[1].明胶酶均是以无活性的酶原形式分泌的,在卵巢的生理活动中,仅有少量的明胶酶被活化,从而发挥作用,但在病理状态下,明胶酶的活化与抑制的平衡被打破,大量活化的明胶酶直接参与肿瘤的侵袭和转移.组织基质金属蛋白酶抑制物(tissue inhibitors of matrix metalloproteinases, TIMPs)可以特异性地抑制明胶酶的活化,是明胶酶天然的抑制剂.本研究采用半定量逆转录聚合酶链反应(RT-PCR)的方法,研究TIMPs与MMP-2、9基因在卵巢上皮性肿瘤(卵巢肿瘤)中的表达及其临床意义.
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Over the past two decades, many investigators have reported how extracellular matrix molecules act to regulate neuroplasticity. The majority of these studies involve proteins which are targets of matrix metalloproteinases. Importantly, these enzyme/substrate interactions can regulate degenerative and regenerative phases of synaptic plasticity, directing axonal and dendritic re-organization after brain insult. The present review ifrst summarizes literature support for the prominent role of matrix metalloproteinases during neuroregeneration, followed by a discussion of data contrasting adaptive and maladaptive neuroplasticity that reveals time-dependent metal-loproteinase/substrate regulation of postinjury synaptic recovery. The potential for these enzymes to serve as therapeutic targets for enhanced neuroplasticity after brain injury is illustrated with experiments demonstrating that metalloproteinase inhibitors can alter adaptive and maladaptive outcome. Finally, the complexity of metalloproteinase role in reactive synaptogenesis is revealed in new studies showing how these enzymes interact with immune molecules to mediate cellu-lar response in the local regenerative environment, and are regulated by novel binding partners in the brain extracellular matrix. Together, these different examples show the complexity with which metalloproteinases are integrated into the process of neuroregeneration, and point to a promising new angle for future studies exploring how to facilitate brain plasticity.
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基质金属蛋白酶及金属蛋白酶组织抑制因子与大肠癌转移的相关性研究
侵袭和转移是恶性肿瘤患者死亡的主要原因,在此过程中基质金属蛋白酶(matrix metalloproteinases,MMPs)参与肿瘤细胞对基底膜(basement membrane,BM)和细胞外基质(extracellular matrix,ECM)的降解,金属蛋白酶组织抑制因子(tissue inhibitors of matrix metalloproteinases,TIMPs)对MMPs的活性起抑制性调节作用.MMPs和TIMPs的平衡是影响肿瘤演进的重要因素.本研究应用免疫组织化学染色方法对大肠癌进行MMP-2、MMP-9和TIMP-1、TIMP-2染色,以探讨MMPs和TIMPs与大肠癌转移的关系.
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膜型基质金属蛋白酶-1在圆锥角膜中表达的研究
本研究通过免疫组织化学法观察正常角膜、圆锥角膜及角膜白斑中膜型基质金属蛋白酶-1(memberane type-1 matrix metalloproteinases,MT1-MMP)的表达,探讨MT1-MMP在圆锥角膜发生发展中的作用.
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基质金属蛋白酶及其组织抑制物在心室重构中的研究
急性冠脉综合征(Acute Coronary Syndrome,ACS)是临床常见的心血管急症,是一组有关急性心肌缺血的临床表现总称,其发病的共同病理基础是冠状动脉内粥样斑块破裂、表面破损或出现裂痕,继而引发不同程度的血栓形成和远端血管栓塞,引起冠状动脉不完全或完全性阻塞.
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Plasmin/plasminogen activators (PA) are the serine enzyme which digests fibrin and/or fibrinogen. Plasmin is produced by the cleavage of its precursor, plasminogen by PAs (urokinase-type PA and tissue-type PA). These events are expected in the thrmbolytic therapy for thromboembolic deseases. Apart from the blood fibrinolysis mentioned above, new role of plasmin/plasminogen activators has been extensively investigated in the field of cellular biology. On the cell surface, the receptor for urokinase-type PA (u-PAR) was found (that for t-PA has not cloned yet). Then, plasmin as well as u-PA itself activates pro-form of matrix metalloproteinases (MMPs) around the pericellular space. These proteolytic activities by u-PA, plasmin and MMPs induce the degradation of extracellular matrix (ECM), affording the cells certain enviroment for their biological function. Further, the coupling of u-PA/u-PAR system and integrins can generate intracellular signal transductions which take part in the regulation of cell proliferation, attachment or migration followed by various physiological and pathophysiological functions. These serial mechanisms are the principle of pericellular proteolytic cascade.
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Cellular chemokine CCL18increases matrix metalloproteinases expression and promotes ovarian cancer cell invasion and metastasis in vivo
Objective:To study the effect of cell chemokine (C-C motif) ligand 18 (CCL18) on ovarian cancer proliferation and metastasis.Methods:This study first analyzed the effects of overexpression of CCL18 on the growth in a subcutaneous ovarian cancer xenografts mouse model.Real-time quantitative PCR was used to detect the expression of matrix metalloproteinases (MMPs) in xenografts tissues.Then,an ovarian cancer orthotropic xenografts model was used to access the effect of CCL18 on ovarian cancer metastasis.Results:Over expressing CCL18 in SKOV3 cells did not significantly promote the tumor growth of subcutaneous xenografts.But the mRNA levels of MMP1,MMP7,MMP11 and MMP15 were significantly inncreased (P < 0.05).The mRNA level of MMP12 was not changed (P >0.05).In orthotopic xenografts ovarian cancer mouse model,metastasis appeared in more organs in CCL 18 overexpressed SKOV3 cells than GFP/SKOV3 cells.Conclusion:CCL18 increased the expresston of MMPs in ovarian cancer cells and promoted metastasis of ovarian cancer cells in vivo.
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膀胱癌患者血清、尿液及组织基质金属蛋白酶及其抑制剂的变化
目的:研究膀胱癌患者血清、尿液及组织基质金属蛋白酶及其抑制剂的变化情况.方法:选取本院收治的64例膀胱癌患者为观察组,另选取64例同期的膀胱良性病变患者为对照组,然后将两组的血清、尿液及组织基质金属蛋白酶及其抑制剂进行检测及比较,并比较观察组中不同分类与分期患者的检测结果.结果:观察组基质金属蛋白酶及其抑制剂的血清、尿液水平和组织阳性率均高于对照组,且不同分期者之间比较,差异具有统计学意义(P<0.05);而观察组中不同分类者比较,差异无统计学意义(P>0.05).结论:膀胱癌患者血清、尿液及组织基质金属蛋白酶及其抑制剂均呈现高表达状态,并且疾病的诊断及治疗效果的监测均有较高的临床价值.