细胞凋亡与肿瘤

细胞凋亡是一种细胞主动性死亡，与组织自稳机制有关。近年来，细胞凋亡在肿瘤发生发展过程中的生物学作用得到普遍重视。研究表明，不仅肿瘤细胞凋亡可受抗癌化疗、放疗等多种因素和途径诱导产生，而且某些肿瘤基因或肿瘤抑制基因，如ｂｃｌ┐２，ｐ５３等对细胞凋亡起重要调控作用     

线粒体与细胞凋亡

细胞凋亡是一种由基因控制的细胞自杀性死亡过程 ,近年来成为生物学、医学领域的一个热点。通过对凋亡机制深入的研究 ,人们发现线粒体的改变已不仅是凋亡的特征 ,还是凋亡调控的中心环节。     

细胞凋亡

论述了细胞凋亡的形态特征及生物学意义 ;阐述了细胞凋亡的基因调控。细胞凋亡是多细胞动物生命现象的自然属性之一 ,是自然的有规律的基因指导下的生物学程序化过程。一旦细胞自然凋亡规律失常 ,机体将发生病变 ,甚至死亡。因此 ,认识细胞凋亡的规律 ,揭示细胞凋亡的机理 ,对指导医学实践 ,提高人们健康水平有极其重要的意义     

Smac、XIAP与细胞凋亡

细胞凋亡是由基因控制的细胞自主有序的死亡.其过程涉及基因的激活、表达和调控等.Smac是一种促凋亡因子,能与凋亡抑制蛋白家族中的XIAP相互作用,共同参与凋亡的调控.本文就Smac和XIAP在细胞凋亡中的作用作一简要综述.     

肿瘤抑制基因与细胞凋亡

肿瘤抑制基因ｐ５３，Ｒｂ，ｐ１６，ｎｍ２３等参与调控肿瘤细胞等多种细胞的凋亡。它们既具有单一的调节作用，又具有复杂的协同效应。研究这些基因在细胞凋亡中的调控机制，对利用基因治疗技术治疗恶性肿瘤具有重要意义     

神经细胞凋亡调控的研究进展

细胞凋亡是机体正常发育过程中普遍存在的生命现象，神经系统的发育也不例外。细胞凋亡与细胞增殖同等重要，二者的动态平衡保证了神经系统的正常发育。近年来研究发现，细胞凋亡受到细胞内多种基因以及细胞外因素的调控。本文就细胞凋亡的生物学特征、基因调控及其与细胞周期的关系等几方面进行了综述     

细胞凋亡与心脏发育关系的研究进展

心脏的发育是原始心源性细胞分化、迁移,多细胞组合的一个精确、协调一致的过程。此变化过程伴随着细胞的凋亡,并受一系列基因的调控。若基因失调控,将引起凋亡异常,结果将导致胚胎心脏异常发育,甚至致畸。通过研究基因表达对细胞凋亡的影响,探讨细胞凋亡与胚胎心脏发育间的关系及影响,阐明胚胎心脏发育过程中的相关机制,能为临床心脏疾病的诊治提供理论基础。     

细胞凋亡的基因调控及应用展望

细胞凋亡的基因调控及应用展望１苏长青综述２龚西马俞审校作者单位：１南京八一医院电镜室，南京２１０００２２安徽医科大学病理学教研室，合肥２３００３２目前，虽然对细胞凋亡的激发与抑制的详细机制还不十分清楚，但已有许多研究资料证实，有多种基因参与了细胞凋亡...     

细胞凋亡的调控与Ⅰ型糖尿病

细胞凋亡(apoptosis),也称程序化死亡,是由基因调控的细胞主动死亡过程.它在调控机体发育,维护内环境稳定,组织形型中起重要作用.Ⅰ型糖尿病是由于各种凋亡调控机制失衡,从而激发胰岛β细胞凋亡加速,导致胰岛丧失大量的分泌功能的一种自身免疫性疾病(autoimmune disease,AID).近年来的研究表明,细胞凋亡与Ⅰ型糖尿病的发病机制有关.本文简要综述细胞凋亡及其调控与Ⅰ型糖尿病之间的关系.     

癫痫中细胞凋亡发生的多元调节机制

细胞凋亡是受到包括基因在内多因素调控的主动性细胞死亡过程,是在多种内外部信号刺激下细胞内部机制被激活进而导致细胞自我毁灭的过程。在癫痫过程中,NMDA受体激活、细胞内Ca2 超载以及基因表达的异常等各种因素相互作用,导致神经元凋亡,本文综述了癫痫过程中导致神经元凋亡发生的多种因素。     

The pathogenesis of inflammatory muscle diseases: on the cutting edge among the environment,the genetic background,the immune response and the dysregulation of apoptosis

Inflammatory muscle diseases (IMD), including dermatomyositis (DM) and polymyositis (PM), affect skeletal muscle, leading to profound tissue modification. The etiology of IMD is unknown, but multiple steps of the disease pathogenesis have been identified. The main alterations involve the immune response. Cellular infiltrates found in the muscle provide strong evidence for the involvement of a preferential immune mechanism of muscle damage. The pathologic differences found between PM and DM indicate a different role played by cell-mediated and humoral immune alterations. It is well accepted that in the pathogenetic pathway both host genes and environmental factors are involved. Apoptosis, or programmed cell death, is a complex process that plays a key role in many physiological events. It regulates the turnover of immune cells and is one of the mechanisms involved in ensuring a competent, non-autoreactive repertoire of lymphocytes. Apoptosis as a mechanism of muscle fibre death has been described in several neuromuscular disorders and muscular dystrophies, and evidence of a lack of apoptosis in IMD suggests a failure of apoptotic clearance of inflammatory cells playing a role in the maintenance of chronic cytotoxic muscle fibre damage. Most likely, the failure of apoptosis seems to be the main hallmark of the pathogenesis of IMD.     

DNA methylation and apoptosis

DNA methylation is an epigenetic phenomenon known to play an increasingly important role in the etiology of cancer. Changes in DNA methylation patterns particularly in the promoter region of genes either in the form of hypomethylation or hypermethylation can have profound effects on gene expression. Hypermethylation in the promoter region of genes is involved in down regulation of the gene expression. Studies from various cancers have revealed that DNA methylation affects genes involved in different cellular pathways including apoptosis. Apoptosis or programmed cell death plays a vital role in the maintenance of cellular homeostasis, i.e. a balance between cell proliferation and cell death. Cancer cells are known to harbor defects in apoptotic pathway and disruption of apoptosis is considered as an important factor aiding its evolution. Evidence from literature indicates that DNA methylation mediated down regulation of genes involved in apoptosis could be a significant mechanism through which tumor cells avoid apoptosis.     

Regulation and execution of apoptosis during Drosophila development.

The development of the Drosophila embryo into an adult fly is a process that integrates cell proliferation and differentiation with programmed cell death, or apoptosis. Apoptosis is an evolutionarily conserved process that is controlled in the developing fly by the products of the genes reaper, grim, and hid. We discuss the role of programmed cell death in the establishment and maintenance of correct patterning in the embryo, and examine the coordination of apoptosis with the hormonally controlled degeneration of larval tissues during metamorphosis. Finally, we address the architecture of the adult eye as an example of how programmed cell death plays a key role in the development of many adult structures.     

Death ligand-mediated apoptosis in HIV infection

Apoptosis has been suggested to cause severe CD4+ T cell depletion in patients infected with HIV. This review focuses on the biological events involved in death ligand-induced apoptosis during HIV infection. Among these ligands, TRAIL appears critical in HIV-infection. Death ligand-induced apoptosis might be a major pathogenic event in many virus-induced diseases including AIDS and the clarification of its mechanism will aid in the development of therapeutic strategies.     

Polymorphisms in apoptosis-related genes and TP53 mutations in non-small cell lung cancer

Apoptosis plays an essential role in the elimination of mutated or transformed cells from the body. Therefore, polymorphisms of apoptosis-related genes may lead to an alteration in apoptotic capacity, thereby affecting the occurrence of TP53 mutations in lung cancer. We investigated the relationship between potentially functional polymorphisms of apoptosis-related genes and TP53 mutations in non-small cell lung cancer (NSCLC). Twenty-seven single nucleotide polymorphisms in 20 apoptosis-related genes were genotyped by a sequenome mass spectrometry-based genotyping assay in 173 NSCLCs and the associations with TP53 mutations in the entire coding exons (exons 2-11), including splicing sites of the gene, were analyzed. None of the 27 polymorphisms was significantly associated with the occurrence of TP53 mutations. This suggests that apoptosis-related genes may not play an important role in the occurrence of TP53 mutations in lung cancer.     

Monogenic syndromes of abnormal glucose homeostasis: clinical review and relevance to the understanding of the pathology of insulin resistance and beta cell failure

Type 2 diabetes mellitus is caused by a combination of insulin resistance and beta cell failure. The polygenic nature of type 2 diabetes has made it difficult to study. Although many candidate genes for this condition have been suggested, in most cases association studies have been equivocal. Monogenic forms of diabetes have now been studied extensively, and the genetic basis of many of these syndromes has been elucidated, leading to greater understanding of the functions of the genes involved. Common variations in the genes causing monogenic disorders have been associated with susceptibility to type 2 diabetes in several populations and explain some of the linkage seen in genome-wide scans. Monogenic disorders are also helpful in understanding both normal and disordered glucose and insulin metabolism. Three main areas of defect contribute to diabetes: defects in insulin signalling leading to insulin resistance; defects of insulin secretion leading to hypoinsulinaemia; and apoptosis leading to decreased beta cell mass. These three pathological pathways are reviewed, focusing on rare genetic syndromes which have diabetes as a prominent feature. Apoptosis seems to be a final common pathway in both type 1 and type 2 diabetes. Study of rare forms of diabetes may help ion determining new therapeutic targets to preserve or increase beta cell mass and function.     

Radiation-induced apoptosis of human peripheral T cells: analyses with cDNA expression arrays and mitochondrial membrane potential assay

We examined sequential changes in post-irradiated peripheral blood T cells taken from normal volunteers, by using targeted Atlas cDNA Expression Arrays and mitochondrial membrane potential assay. At 1 and 3 hours after 5 Gy irradiation, changes of gene expression were examined by targeted Atlas cDNA Expression Arrays using Apoptosis Array. The Atlas Human Apoptosis Array includes 205 key genes that are known to control apoptosis, including extracellular and cytoplasmic effectors. Concerning Fas, no significant changes of spot intensities were identified between irradiated T cells and non-irradiated ones at both 1 h and 3 h after 5 Gy irradiation. Caspase families, including caspases 9 and 3 also showed no changes between these two groups. An apoptosis regulator bclw showed a remarkable decrease in irradiated T cells. These results suggested that irradiation induced direct apoptosis of T cells by changing the membrane potential of mitochondria. Using a CCD camera-equipped fluorescence microscope and MitoCapture, a mitochondrial membrane potential indicator, we demonstrated 5 Gy radiation induced loss of membrane potential, i.e., an early stage of apoptosis, in human peripheral blood T cells at 10 hours after irradiation.     

细胞凋亡及其相关基因在冷灌注保存大鼠肝脏组织中的作用

目的通过检测凋亡细胞计数及凋亡相关基因bax和Fas的表达。探讨细胞凋亡及其相关基因在冷灌注保存大鼠肝脏组织中的作用。方法本研究采用脱氧核糖核苷酸末端转移酶介导的末端标记法（TUNEL法）及RT-PCR．按照供肝保存时间30、60、90、120、180、300min分为6组进行凋亡细胞计数及其相关基因的检测。结果不同保存时间大鼠肝脏组织中均有凋亡细胞发生。随着时间延长，凋亡细胞计数呈进行性增加趋势；未检测到bcl-2的表达．但可明显检测到bax和Fas基因的表达。结论在冷灌注保存肝组织中，细胞凋亡是早期细胞死亡的主要原因之一。细胞凋亡的发生可能与bax和Fas的高表达以及bcl-2的低表达有关。