共查询到19条相似文献,搜索用时 421 毫秒
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微粒是血管内皮细胞、组织细胞或血细胞激活或凋亡时形成的亚微型囊泡。动脉粥样硬化时血浆及粥样斑块中富含多种细胞来源的微粒,不仅促进斑块的发生发展并且在动脉粥样硬化凝血异常中起重要作用,可增进血管内皮细胞和白细胞间的相互作用,使单核细胞粘附于内皮细胞,从而迁移到斑块内,吞噬清除内膜下沉积的脂质。巨噬细胞吞噬脂质后凋亡形成大量微粒,抑制内皮细胞合成释放一氧化氮,加重内皮细胞损伤,促进斑块扩大。微粒表面富含的磷脂酰丝氨酸和组织因子是微粒促凝活性的主要来源,病灶处及循环中存在的大量微粒促进了动脉粥样硬化时凝血异常的发生。本文将就微粒在动脉粥样硬化形成及凝血异常中的作用做一综述。 相似文献
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氧化修饰在调控细胞凋亡信号转导中的作用 总被引:2,自引:0,他引:2
氧化修饰是细胞内的活性氧诱导生物大分子发生氧化反应引起的结构及构象改变,发挥调控信号转导和对应激作出反应的功能。氧化修饰发生在凋亡信号转导中的多个生物大分子,包括凋亡相关蛋白质的氧化,如caspase-9、线粒体通透性转变孔及电压依赖的阴离子通道(voltagedependent anion channel,VDAC),同时也包括膜磷脂的氧化修饰,如磷脂酰丝氨酸及线粒体特异的心磷脂。氧化修饰作用也涉及凋亡诱导因子、促凋亡的凋亡信号调控激酶1(apoptosis signalregulatin gkinasel,ASK1)信号转导途径及抗凋亡的转录因子NF—kB的激活和活性。所以氧化修饰可能是调控凋亡信号转导机制中除磷酸化、泛素化外的另一个新的分子机制。 相似文献
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细胞衰老是指细胞在各种应激条件下出现周期阻滞,不可逆地丧失增殖能力,其形态、基因表达和功能都发生特定变化的过程。研究表明,血管内皮细胞衰老可以通过削弱血管功能,促进衰老相关血管疾病的发生发展。然而,有关内皮细胞衰老的发生机制以及内皮细胞衰老影响血管功能及衰老相关血管疾病的潜在机制尚待挖掘。本文从血管内皮细胞衰老相关的信号通路,以及血管内皮细胞衰老与血管功能和血管相关疾病(动脉粥样硬化、高血压和糖尿病血管并发症)的最新研究进展进行综述,为进一步认识血管疾病的发病机制,延缓血管衰老提供新的思路。 相似文献
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炎症小体是细胞内组装形成的大分子蛋白复合体,可将白介素-1β(IL-1β) 和IL-18 加工成熟,并诱导细胞焦亡性死亡,在协调对抗病原体感染和生理紊乱的过程中发挥重要作用。Nod 样受体蛋白3(Nod-like receptor protein 3, NLRP3) 炎症小体是迄今为止结构和功能研究得最为明确的炎症小体,其活化后参与免疫性疾病、心血管疾病、神经系统疾病等多种疾病发生及发展过程。研究显示,许多中药有效成分可以调节相关疾病靶细胞中NLRP3 炎症小体的活化。从中药有效成分调节相关疾病靶细胞(如神经细胞、肝肾细胞、内皮细胞、肿瘤细胞等)中NLRP3 炎症小体活化的机制出发,综述近4 年国内外对中药有效成分调节NLRP3 炎症小体活化的研究进展,以期阐释相关中药有效成分的作用特点,并为相关疾病的防治提供一定参考。 相似文献
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分子探针应用于细胞凋亡检测具有直观、无创伤和实时动态观察凋亡分子信息的特点,在疾病早期诊断、监测疾病发展进程、评估疾病治疗效果、发展新的治疗方案等方面具有较好的应用前景.综述了近年来靶向细胞凋亡探针的设计、作用机制、应用等相关的研究进展,并根据亲和组件的作用机制对分子探针进行分类介绍. 相似文献
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Loïc Doeuvre† Laurent Plawinski‡ Florence Toti§¶ Eduardo Anglés-Cano 《Journal of neurochemistry》2009,110(2):457-468
Microparticles (MPs) are membrane fragments shed by cells activated by a variety of stimuli including serine proteases, inflammatory cytokines, growth factors, and stress inducers. MPs originating from platelets, leukocytes, endothelial cells, and erythrocytes are found in circulating blood at relative concentrations determined by the pathophysiological context. The procoagulant activity of MPs is their most characterized property as a determinant of thrombosis in various vascular and systemic diseases including myocardial infarction and diabetes. An increase in circulating MPs has also been associated with ischemic cerebrovascular accidents, transient ischemic attacks, multiple sclerosis, and cerebral malaria. Recent data indicate that besides their procoagulant components and identity antigens, MPs bear a number of bioactive effectors that can be disseminated, exchanged, and transferred via MPs cell interactions. Furthermore, as activated parenchymal cells may also shed MPs carrying identity antigens and biomolecules, MPs are now emerging as new messengers/biomarkers from a specific tissue undergoing activation or damage. Thus, detection of MPs of neurovascular origin in biological fluids such as CSF or tears, and even in circulating blood in case of blood–brain barrier leakage, would not only improve our comprehension of neurovascular pathophysiology, but may also constitute a powerful tool as a biomarker in disease prediction, diagnosis, prognosis, and follow-up. 相似文献
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Heba El-Gamal Aijaz S. Parray Fayaz A. Mir Ashfaq Shuaib Abdelali Agouni 《Journal of cellular physiology》2019,234(10):16739-16754
Stroke is one of the leading causes of mortality and disability worldwide. Numerous pathophysiological mechanisms involving blood vessels, coagulation and inflammation contribute to the vascular occlusion. Perturbations in these pathways can be detected by numerous methods including changes in endoplasmic membrane remodeling and rearrangement leading to the shedding of microparticles (MPs) from various cellular origins in the blood. MPs are small membrane-derived vesicles that are shed from nearly all cells in the body in resting state or upon stimulation. MPs act as biological messengers to transfer information to adjacent and distant cells thus regulating various biological processes. MPs may be important biomarkers and tools for the identification of the risk and diagnosis of cerebrovascular diseases. Endothelial activation and dysfunction and altered thrombotic responses are two of the main features predisposing to stroke. Endothelial MPs (EMPs) have been recognized as both biomarkers and effectors of endothelial cell activation and injury while platelet-derived MPs (PMPs) carry a strong procoagulant potential and are activated in thrombotic states. Therefore, we reviewed here the role of EMPs and PMPs as biomarkers of stroke. Most studies reported high circulating levels of EMPs and PMPs in addition to other cell origins in stroke patients and have been linked to stroke severity, the size of infarction, and prognosis. The identification and quantification of EMPs and PMPs may thus be useful for the diagnosis and management of stroke. 相似文献
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P Zordan E Rigamonti K Freudenberg V Conti E Azzoni P Rovere-Querini S Brunelli 《Cell death & disease》2014,5(1):e1031
The damage of the skeletal muscle prompts a complex and coordinated response that involves the interactions of many different cell populations and promotes inflammation, vascular remodeling and finally muscle regeneration. Muscle disorders exist in which the irreversible loss of tissue integrity and function is linked to defective neo-angiogenesis with persistence of tissue necrosis and inflammation. Here we show that macrophages (MPs) are necessary for efficient vascular remodeling in the injured muscle. In particular, MPs sustain the differentiation of endothelial-derived progenitors to contribute to neo-capillary formation, by secreting pro-angiogenic growth factors. When phagocyte infiltration is compromised endothelial-derived progenitors undergo a significant endothelial to mesenchymal transition (EndoMT), possibly triggered by the activation of transforming growth factor-β/bone morphogenetic protein signaling, collagen accumulates and the muscle is replaced by fibrotic tissue. Our findings provide new insights in EndoMT in the adult skeletal muscle, and suggest that endothelial cells in the skeletal muscle may represent a new target for therapeutic intervention in fibrotic diseases. 相似文献
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Fabiana K. Marques Fernanda M. F. Campos Lirlândia P. Sousa Andréa Teixeira-Carvalho Luci M. S. Dusse Karina B. Gomes 《Molecular biology reports》2013,40(7):4553-4559
Preeclampsia (PE) is a syndrome characterized by poor placentation and endothelial dysfunction. The diagnosis for this syndrome is based in hypertension and proteinuria presented after the 20th week of pregnancy. Despite intensive research, PE is still one of the leading causes of maternal mortality, although reliable screening tests or effective treatments of this disease have yet to be proposed. Microparticles (MPs) are small vesicles released after cell activation or apoptosis, which contain membrane proteins that are characteristic of the original parent cell. MPs have been proven to play key role in thrombosis, inflammation, and angiogenesis, as well as to mediate cell–cell communication by transferring mRNAs and microRNA from the cell of origin to target cells. Placenta-derived syncytiotrophoblast MPs are one of the most increased MPs during PE and may play an important role in the pathogenesis of this syndrome. Therefore, a better overall understanding of the role of MPs in PE may be useful for new clinical diagnoses and therapeutic approaches. 相似文献
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Mostefai HA Agouni A Carusio N Mastronardi ML Heymes C Henrion D Andriantsitohaina R Martinez MC 《Journal of immunology (Baltimore, Md. : 1950)》2008,180(7):5028-5035
Microparticles (MPs) are membrane vesicles released during cell activation and apoptosis. We have previously shown that MPs from apoptotic T cells induce endothelial dysfunction, but the mechanisms implicated are not completely elucidated. In this study, we dissect the pathways involved in endothelial cells with respect to both NO and reactive oxygen species (ROS). Incubation of endothelial cells with MPs decreased NO production that was associated with overexpression and phosphorylation of endothelial NO synthase (eNOS). Also, MPs enhanced expression of caveolin-1 and decreased its phosphorylation. Microparticles enhanced ROS by a mechanism sensitive to xanthine oxidase and P-IkappaBalpha inhibitors. PI3K inhibition reduced the effects of MPs on eNOS, but not on caveolin-1, whereas it enhanced the effects of MPs on ROS production. Microparticles stimulated ERK1/2 phosphorylation via a PI3K-depedent mechanism. Inhibition of MEK reversed eNOS phosphorylation but had no effect on ROS production induced by MPs. In vivo injection of MPs in mice impaired endothelial function. In summary, MPs activate pathways related to NO and ROS productions through PI3K, xanthine oxidase, and NF-kappaB pathways. These data underscore the pleiotropic effects of MPs on NO and ROS, leading to an increase oxidative stress that may account for the deleterious effects of MPs on endothelial function. 相似文献
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Though stem cell transplantation has been confirmed to be useful in repairing aging and diseased tissues, the underlying mechanism remains elusive. In addition to soluble molecules, cells-derived membrane microparticles (MPs) are considered as new mediators served in cross-talk communication among cells. MPs are tiny membrane coated subcellular vesicles released by a variety of cell types including stem cells. MPs may interact with target cells through specific receptor-ligand interactions and transfering proteins, bioactive lipids, mRNA and miRNA. Composition and function of stem cells derived MPs are highlighted in recent years. Here, we give an overview of MPs'composition, vesiculation and liberation mechanism, roles involved in communication exchages, and research progress in stem cells derived MPs. The report here might provide some novel information to highlight the stem cells therapy. 相似文献
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Takahiko Tanigawa Hisao Takayama Hitoshi Osatake Keiichi Tanaka Noriko Kasagi Yoshinori Tanaka 《Cytotechnology》1992,10(1):43-51
Characteristics of mouse macrophage (MP) cell lines A640-BB-2, J774.1 and P388D1 and mouse peritoneal exudate MPs were studied and compared in cell morphology, ability to recognize tumor cells in the presence and absence of OK-432 known to activate MPs, and in lysosomal enzyme activity. In A640-BB-2 cells and exudate MPs, cell surfaces showed a few ridge-like processes and microvilli; spontaneous cytotoxicity was moderate against tumor target L929, and little or absent against targets SV3T3, B-16 and U937; and lysosomal enzyme activity of nonspecific esterase, acid phosphatase, and -glucuronidase was high. After culture in the presence of OK-432, A640-BB-2 cells and exudate MPs showed more extensive spreading with larger surface areas and with increased numbers of ridge-like processes and microvilli, and their cytotoxicity against target L929 became more extensive. The stable soluble factor did not participate in the mechanism of cytotoxicity against target L929 mediated by A640-BB-2 cells and exudate MPs. J774.1 and P388D1 cells were different from exudate MPs in cell morphology and ability to recognize tumor cells when cultured either with or without OK-432, and in lysosomal enzyme activity. A640-BB-2 cells seem to be useful in studying MP-tumor cell interaction and MP activation, and in detecting the trace biological activating factor of MPs.Abbreviations DEM
Dulbecco's modified Eagle's medium
- MP
macrophage
- PBS
phosphate-buffered saline
- SEM
scanning electron microscopy 相似文献
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McVey M Tabuchi A Kuebler WM 《American journal of physiology. Lung cellular and molecular physiology》2012,303(5):L364-L381
The pathophysiology of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), is characterized by increased vascular and epithelial permeability, hypercoagulation and hypofibrinolysis, inflammation, and immune modulation. These detrimental changes are orchestrated by cross talk between a complex network of cells, mediators, and signaling pathways. A rapidly growing number of studies have reported the appearance of distinct populations of microparticles (MPs) in both the vascular and alveolar compartments in animal models of ALI/ARDS or respective patient populations, where they may serve as diagnostic and prognostic biomarkers. MPs are small cytosolic vesicles with an intact lipid bilayer that can be released by a variety of vascular, parenchymal, or blood cells and that contain membrane and cytosolic proteins, organelles, lipids, and RNA supplied from and characteristic for their respective parental cells. Owing to this endowment, MPs can effectively interact with other cell types via fusion, receptor-mediated interaction, uptake, or mediator release, thereby acting as intrinsic stimulators, modulators, or even attenuators in a variety of disease processes. This review summarizes current knowledge on the formation and potential functional role of different MPs in inflammatory diseases with a specific focus on ALI/ARDS. ALI has been associated with the formation of MPs from such diverse cellular origins as platelets, neutrophils, monocytes, lymphocytes, red blood cells, and endothelial and epithelial cells. Because of their considerable heterogeneity in terms of origin and functional properties, MPs may contribute via both harmful and beneficial effects to the characteristic pathological features of ALI/ARDS. A better understanding of the formation, function, and relevance of MPs may give rise to new promising therapeutic strategies to modulate coagulation, inflammation, endothelial function, and permeability either through removal or inhibition of "detrimental" MPs or through administration or stimulation of "favorable" MPs. 相似文献
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Rajesh Ramakrishnan Hongbing Liu Hart Donahue Anna Malovannaya Jun Qin Andrew P Rice 《Retrovirology》2012,9(1):1-14