Caspase家族与细胞凋亡的关系

凋亡是导致细胞死亡的调节性生理过程。Caspase半胱氨酸蛋白酶家族引发的级联反应是细胞凋亡过程的中心环节,其激活主要包括线粒体依赖途径和死亡受体介导的信号转导途径,激活后的下游Caspase,通过切割特异性底物,导致细胞凋亡。现以Caspase家族与细胞凋亡的关系为主,对Caspase基因家族生物学特性、调控细胞凋亡的分子机制进行综述。     

细胞凋亡在肾脏疾病中的作用

细胞凋亡是基因调控的细胞生理性死亡形式 ,是一种主动、自发性的过程 ,是目前生物学和医学界的研究热点。文章通过对细胞凋亡的形态学、生物化学、免疫化学和分子生物学的检测方法、促进细胞凋亡和抑制细胞凋亡的基因、以及细胞凋亡与肾脏疾病的关联作一综述。旨在阐明细胞凋亡在肾小球肾炎、肾小管疾病以及继发性肾脏疾病等肾脏疾病发病机制中的重要作用     

细胞凋亡的主要检测方法研究进展

细胞凋亡是生理性细胞死亡过程,凋亡在维持动物机体内环境平衡中扮演着极其重要的角色.细胞凋亡的准确检测是研究细胞凋亡相关机制,以及评价细胞凋亡在相应组织或疾病中影响的第一步.形态学是检测细胞凋亡的最直观的方法,至今一直作为细胞凋亡检测的金标准.DNA片段化检测主要有DNA ladder,TUNEL检测法和ELISA检测法...     

猪繁殖与呼吸综合征感染与细胞凋亡的研究进展

细胞凋亡是指在一定的生理或病理情况下,机体为维护内环境的稳定,通过基因调控,激活内源性核酸内切酶,发生细胞自动消亡的过程。研究猪繁殖与呼吸综合征（PRRSV）感染与细胞凋亡的关系及凋亡的可能机制将有助于人们认识PRRSV感染性的发生、发展及转归机制,现综述国内外近年来对PRRSV诱导细胞凋亡的相关研究进展,为进一步阐明PRRSV的致病机制和该病的防治提供一些新的思路。     

动物胎盘细胞凋亡的研究进展

细胞凋亡是由基因编码决定的细胞主动死亡,参与机体生理过程及疾病的发生过程。胎儿的生长发育是一个极其复杂的生理过程,在此妊娠过程中胎盘的细胞增殖和凋亡之间处于不同的平衡状态,这种状态一旦被破坏就会出现不同的病理妊娠症状。本文对影响动物胎盘细胞凋亡的因素、正常的胎盘细胞凋亡、胎盘细胞凋亡对妊娠和胎儿发育的影响进行了综述。     

细胞凋亡信号传导通路的研究进展

细胞凋亡是多细胞生物调控生物体的发育、细胞更新和维持内环境稳定的一种重要机制。目前发现细胞凋亡存在死亡受体通路、线粒体通路和内质网通路3条通路,且各通路之间相互联系,共同促进细胞凋亡。作者综述了近年来细胞凋亡信号传导通路及其调控的研究进展。     

Caspase非依赖性细胞死亡的研究进展

细胞凋亡是一种生理性细胞死亡机制，它是由多基因调控的一种细胞的主动的自杀性过程。一般认为它是由蛋白酶caspases通过两种途径激活的。但是，近年来研究发现除caspases引起的细胞凋亡外，还有caspases非依赖性的细胞死亡形式存在，包括细胞的自我吞噬作用、细胞蛋白酶体的降解和线粒体途径。这些途径无论是在试验的条件下还是在生理或病理的情况下都可以观察到。目前认为凋亡诱导因子(AIF)在caspases非依赖性的细胞死亡中起关键作用。     

Morphological and biochemical aspects of apoptosis,oncosis and necrosis

Recent investigations have demonstrated the need for a precise differentiation of various forms of cell death such as apoptosis, oncosis, necrosis and programmed cell death. Apoptosis is marked by cellular shrinking, condensation and margination of the chromatin and ruffling of the plasma membrane with eventually breaking up of the cell in apoptotic bodies. Cell death marked by cellular swelling should be called oncosis, whereas the term necrosis refers to the morphological alterations appearing after cell death. Apoptosis and oncosis are therefore pre-mortal processes, while necrosis is a post-mortal condition. The term programmed cell death refers to the 'fixed' pathway followed by dying cells, whether or not with the characteristic morphology of apoptosis. Three mechanisms are actually known to be involved in the apoptotic process: a receptor-ligand mediated mechanism, a mitochondrial pathway and a mechanism in which the endoplasmic reticulum plays a central role. All three mechanisms activate caspases which are responsible for the characteristic morphological changes observed during apoptosis. A review of the different methods used for detecting apoptotic cells demonstrates that most of these techniques are not entirely specific.     

家禽免疫器官内细胞凋亡及其凋亡相关基因调控研究进展

细胞凋亡是生物界广泛存在的一种重要的生命过程，是多细胞动物为调节机体发育、维护内环境稳定、有基因调控的细胞主动性死亡过程。在细胞凋亡的分子生物学研究过程中，发现已有多种基因参与细胞凋亡的调控，其中包括Bcl-2家族和Bax、p53、Fas和FasL等。家禽免疫器官胸腺、脾脏和法氏囊内存在着自然凋亡现象，许多学者用物理性、化学性和生物性因素诱导了家禽免疫器官细胞凋亡，证实了细胞凋亡相关基因参与了家禽免疫器官内细胞凋亡的调控。     

Sensitivity of skeletal muscle to pro-apoptotic factors

In mononuclear cells, apoptosis leads to DNA fragmentation and cell destruction, regardless of the activated pathway. As regards multinuclear cells, e.g. skeletal muscle fibers, apoptosis rarely induces the death of the entire cell, and it generally affects single nuclei. This process, referred to as nuclear apoptosis, has a negative effect on the expression of genes in the myonuclear domain. Apoptosis may be initiated in muscle cells by external stimuli which activate cell membrane death receptors as well as by internal stimuli which stimulate the mitochondrial release of pro-apoptotic proteins. Reactive oxygen species also play an important role in the initiation of apoptosis. In muscle cells, ROS are produced in response to extracellular reactions or by cell mitochondria. It is, therefore, believed that mitochondria play a central role in apoptosis within skeletal muscle. Skeletal muscles have a well-developed system that protects them against oxidative damage. Myogenic stem cells are an integral part of multinucleated myofibers, and they are critically important for the maintenance of normal muscle mass, muscle growth, regeneration and hypertrophy. The latest research results indicate that myogenic cells are more sensitive to oxidative stress and pro-apoptotic factors than well-differentiated cells, such as myotubes. The complex structure and activity of skeletal muscle prompted research into the role of apoptosis and its intensity under various physiological and pathological conditions. This review summarizes the results of research investigating control mechanisms and the apoptosis process in skeletal muscle fibers, and indicates unresearched areas where further work is required.     

哺乳动物卵母细胞凋亡的研究现状及新进展

细胞凋亡又称程序性细胞死亡,是指机体为维持体内环境的稳定,由基因控制的细胞自主的有序性死亡。对于雌性生殖系而言,细胞凋亡是维持其正常功能的一个重要组成要术。就哺乳动物来说,超过99．9％的雌性生殖细胞会在发育的不同时期发生凋亡。本文主要综述了细胞凋亡的新概念、卵子发生过程中的细胞凋亡现象,同时还对当今卵母细胞凋亡研究的现状及新进展做出了总结。     

Apoptosis and anti-apoptotic heat shock proteins in canine cutaneous infundibular keratinizing acanthomas and squamous cell carcinomas

Cell stress and death are linked in the neoplastic process, and heat shock proteins appear to play an important role by inhibiting apoptotic pathways. The apoptotic rates in 9 canine infundibular keratinizing acanthomas (IKAs) and 17 canine squamous cell carcinomas (SCCs) were correlated with the immunohistochemical expression of caspase-3 and the antiapoptotic heat shock proteins Hsp27, 72 and 73. Apoptosis was evaluated using the terminal deoxynucleotidyl transferase biotin-dUTP nick end labelling (TUNEL) method. The absence of a correlation between the TUNEL index and active-caspase-3 expression, a paucity of active-caspase-3-positive cells and Hsp72 over-expression were considered to be indicative of inhibition of apoptosis, and suggestive that inhibition of cell death plays a key role in oncogenesis and tumour growth of some canine skin neoplasms.     

细胞凋亡的研究现状与发展趋势

凋亡 ( Ap)是一种细胞死亡的形态学描述。 Ap不但出现在人类生命的全过程 ,也是调节机体生理、病理过程的主要因素之一。它不仅参与生物体的生长发育 ,而且介导了一些疾病的发生和发展。文章介绍了细胞凋亡的分子机制、生物学意义、形态学和生化特征、凋亡途径及基因调控方面的研究进展 ;并通过对 Ap几种检测方法的比较 ,重点分析了常规 HE染色法和TUNEL法在细胞凋亡检测方面的利弊 ;同时对Ap与 AID、肿瘤、病毒感染、神经系统疾病、缺血性损伤等疾病的关系及其研究趋势作了较全面的阐述。     

Advance of Apoptotic Mechanism in Mammalian Oocyte

Apoptosis is programmed cell death process, which plays an important role in the process of development of germ cells. In the process of growth and development of mammalian oocytes, in addition to the mature ovulation fertilization of the oocytes, the others are apoptotic at different stages of follicular oocytes. This paper summarizes the research progress of development of the main apoptosis mechanism and apoptosis pathway of mammalian oocytes, and lays a foundation for further studying growth, development and ovulation mechanism of oocytes.     

哺乳动物卵母细胞凋亡机制研究进展

细胞凋亡是细胞程序性死亡过程,在生殖细胞的发生过程中具有重要作用。哺乳动物卵母细胞在生长发育过程中,除排卵受精的成熟卵母细胞外,其他卵母细胞在卵泡发育的不同阶段凋亡。作者综述了卵母细胞的发育与细胞凋亡、细胞凋亡的主要参与分子及凋亡途径等研究进展,旨在为进一步研究哺乳动物卵母细胞的生长、发育和排卵机制提供帮助。     

细胞凋亡与细胞坏死比较的研究进展

本文对细胞凋亡和细胞坏死的发病机理和病理形态学进行了比较。凋亡是细胞的一种主动性死亡。其特点是单细胞发生,胞核浓缩、破裂,核碎块被胞膜包裹,形成特异性“凋亡小体”;细胞器多以萎缩变化为主。坏死则为细胞的被动性死亡,并常伴有炎症反应。作者认为：细胞凋亡和坏死虽然在发生机制和病理形态学方面有所区别,但它们的本质却是相同的,均为细胞的一种不可复性的退行性变化。     

Role of apoptosis in the pathogenesis of Asian and South American foot-and-mouth disease viruses in swine

In this study, we performed experiments to evaluate the extend of the process of apoptotic cell death by foot-and-mouth disease virus (FMDV). Apoptosis can also occur in some virus-infected cells, and ability of viruses to either inhibit or promote apoptosis may influence the pathologic outcome of infection. In this study, to determine if apoptosis plays a role in the outcome of FMDV infection in swine, we evaluated apoptosis in diseased tissues collected from pigs inoculated with two different stains of FMDV (O1 Campos and O Taiwan). And host cell DNA fragmentation in diseased tissue from animals which were infected with either virus was evaluated by occurrence of a laddering pattern characteristic of apoptosis. Infection of cultured keratinocytes from swine tongue failed to demonstrate apoptosis in the first few hours of infection, suggesting that cell-to-cell correlation between viral antigen and apoptotic changes, e.g. cytokine secretions by immune system cells, could be critical to initiating apoptosis. Consistent with this finding, we were able to detect the pro-inflammatory cytokine TNF-alpha in diseased tissues. A clear difference in the pathogenicity of the two different FMDV isolates to pigs was not demonstrated in our study.     

Apoptosis: A review of pro‐apoptotic and anti‐apoptotic pathways and dysregulation in disease

Objective – To review the human and veterinary literature on the biology of apoptosis in health and disease. Data Sources – Data were examined from the human and veterinary literature identified through Pubmed and references listed in appropriate articles pertaining to apoptosis. Human Data Synthesis – The role of apoptosis in health and disease is a rapidly growing area of research in human medicine. Apoptosis has been identified as a component of human autoimmune diseases, Alzheimer's disease, cancer, and sepsis. Veterinary Data Synthesis – Research data available from the veterinary literature pertaining to apoptosis and its role in diseases of small animal species is still in its infancy. The majority of veterinary studies focus on oncologic therapy. Most of the basic science and human clinical research studies use human blood and tissue samples and murine models. The results from these studies may be applicable to small animal species. Conclusions – Apoptosis is the complex physiologic process of programmed cell death. The pathophysiology of apoptosis and disease is only now being closely evaluated in human medicine. Knowledge of the physiologic mechanisms by which tissues regulate their size and composition is leading researchers to investigate the role of apoptosis in human diseases such as cancer, autoimmune disease and sepsis. Because it is a multifaceted process, apoptosis is difficult to target or manipulate therapeutically. Future studies may reveal methods to regulate or manipulate apoptosis and improve patient outcome.     

Vesicular stomatitis virus infection and neuropathogenesis in the murine model are associated with apoptosis

This study examines apoptosis and viral neuropathogenesis in a murine model infected with vesicular stomatitis virus (VSV). VSV induces apoptotic cell death in cultured cell lines, raising the possibility that apoptosis of infected neurons and other target cells may contribute to disease and mortality. To determine whether or not VSV induces apoptosis in neural tissues, mice were inoculated intranasally with VSV. At 24, 48, 72, 96, and 120 hours postinfection, brain tissues were assayed for the presence of viral RNA by in situ hybridization and viral antigen by immunohistochemistry. Apoptosis was identified by in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling and electron microscopy. Viral replication and lesions were observed predominantly in central nervous system neurons. Apoptotic cell death was restricted to the same regions of the brain in which infected cells and tissue injury were identified. Results suggest that VSV-induced apoptosis is a mechanism causing cell death, tissue injury, and mortality in VSV-infected mice.     

The apoptosis-necrosis continuum: insights from genetically altered mice

Apoptosis can be defined as a carefully regulated process, characterized by specific morphologic and biochemical features. It is initiated by both physiologic and pathologic stimuli, and its full expression requires a signaling cascade in which caspase activation plays a central role. Knockout mice lacking key genes encoding proteins constituting the core apoptotic cascade have helped us to establish the functional hierarchy of the mechanisms controlling apoptosis in animal development and, to a lesser extent, in disease. Induced mutant mice have also revealed the intimate crosstalk between apoptotic and other homeostatic pathways and have defined distinct temporal and tissue-specific roles of individual apoptotic effectors. Eliminating genes controlling caspase-dependent apoptosis can convert an apoptotic phenotype to a necrotic one, both in vitro and in vivo. This suggests that necrosis and apoptosis represent morphologic expressions of a shared biochemical network through both caspase-dependent mechanisms as well as non-caspase-dependent effectors such as cathepsin B and apoptosis-inducing factor. The cell death program, whether by apoptosis or necrosis, is mediated through an integrated cascade, which can be accessed at multiple sites, and propagated through numerous branch points. An understanding of the physiologic conditions that influence these decisions is required to adequately prevent, or induce, cell death.