共查询到20条相似文献，搜索用时 956 毫秒
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Oonuma T Morimatsu M Ochiai K Iwanaga T Hashizume K 《The Journal of veterinary medical science / the Japanese Society of Veterinary Science》2007,69(3):279-284
Molecule possessing ankyrin-repeats induced by lipopolysaccharide (MAIL) is a nuclear IkappaB protein that is also known as interleukin-1-inducible nuclear ankyrin repeat protein and inhibitor of nuclear factor kappaBzeta (IkappaBzeta). We previously observed that MAIL-deficient mice were affected by atopic dermatitis-like skin lesions and demonstrated the importance of MAIL in the skin. In this study, we investigated MAIL expression in mouse keratinocytes. MAIL mRNA was constitutively expressed in the skin epidermis. MAIL expression was also confirmed in primary keratinocytes and the PAM212 keratinocyte cell line. The inhibitors of nuclear factor kappaB (NF-kappaB)-Bay11-7082 and the IkappaBalphaM supersuppressor-considerably downregulated MAIL expression in the keratinocytes. Immunoreactivity for NF-kappaB components was localized in the cytoplasm and nucleus of normal unstimulated keratinocytes. The expression level of MAIL in the skin did not change following lipopolysaccharide (LPS) administration to mice. Interestingly, in accordance with the in vivo findings, the MAIL expression level did not change following LPS stimulation even in primary keratinocytes; however, MAIL expression was strongly increased by interleukin-1 stimulation. These results collectively suggest that the constitutive expression of MAIL in keratinocytes is controlled, at least in part, by NF-kappaB and that there may be LPS-specific repressive mechanisms that inhibit MAIL induction. 相似文献
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自发现细胞核转录因子-κB(NF-κB)以来,人们对其分子生物学特征、作用机制及其与疾病的关系作了广泛的研究。近年来的研究结果发现,NF-κB在病毒感染与疾病发生的过程中发挥着重要作用。病毒感染真核细胞时能诱导NF-κB从细胞质转移到细胞核,从而诱导一些炎性基因转录产生大量炎性因子引起炎症反应,或阻碍细胞凋亡促进其自身在宿主细胞内的复制,或促进某些原癌基因的表达使细胞癌化等。不同病毒感染机体时,都会通过对NF-κB信号转导的影响,改变机体的某些性状,导致疾病的产生。目前已发现应激刺激、细菌脂多糖、病毒、氧自由基等很多因素能激活NF-κB,而后通过NF-κB信号转导通路的桥接作用影响机体的新陈代谢,文章就病毒感染与细胞NF-κB信号转导的相互作用关系作一综述。 相似文献
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Planz O 《Berliner und Münchener tier?rztliche Wochenschrift》2006,119(3-4):101-111
It has been described in the last years that after influenza virus-infection a variety of intracellular signalling pathways have been induced. There are examples and suggestions how the viral replication cycle leads to the activation of intracellular signalling pathways. A variety of signalling pathways are activated after virus-infection as an alert-response against the invading pathogen that can be considered as an antiviral response of the host cell. Nevertheless, it was also shown, that viruses are able to suppress these cellular responses to assure their own replication. Moreover, viruses are also able to activate and misuse cellular signalling pathways for their own survival. The NF-kappaB signalling pathway is an excellent example of these sceneries. Activation of the NF-kappaB signalling pathway mediated by the virus can partially be blocked by the NS1 protein to suppress a strong antiviral IFN alpha/beta response. At the same time the virus takes advantage of the remaining NF-kappaB activity for virus related apoptosis and for its own replication. This is a highly effective and economic way for the virus to control its replication without the need for specific viral inducers of cellular responses. This demonstrates, that there are no "all or nothing" reactions in the field of interactions of Influenza viruses with intracellular signalling pathways. In one situation cellular antiviral responses can be misused by the virus of its own replication and at another point the same signalling pathway may even be turned into a pro-viral activity. When the impact of a given signalling pathway on viral growth is evaluated these bivalent functions of these pathways should be taken in consideration. Nevertheless, a signalling pathway that supports viral growth is an excellent target for antiviral therapy (Ludwig et al. 2003). 相似文献
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Ding L Xu X Huang Y Li Z Zhang K Chen G Yu G Wang Z Li W Tong D 《Veterinary microbiology》2012,158(1-2):12-22
Transmissible gastroenteritis virus (TGEV) has been reported to induce apoptosis in swine testis (ST) cells. However, the mechanisms underlying TGEV-induced apoptosis are still unclear. In this study we observed that TGEV infection induced apoptosis in porcine kidney (PK-15) cells in a time- and dose-dependent manner. TGEV infection up-regulated FasL, activated FasL-mediated apoptotic pathway, leading to activation of caspase-8 and cleavage of Bid. In addition, TGEV infection down-regulated Bcl-2, up-regulated Bax expression, promoted translocation of Bax to mitochondria, activated mitochondria-mediated apoptotic pathway, which in turn caused the release of cytochrome c and the activation of caspase-9. Both extrinsic and intrinsic pathways activated downstream effector caspase-3, followed by the cleavage of PARP, resulting in cell apoptosis. Moreover, TGEV infection did not induce significant DNA fragmentation in ammonium chloride (NH(4)Cl) pretreated PK-15 cells or cells infected with UV-inactivated TGEV. In turn, block of caspases activation also did not affect TGEV replication. Taken together, this study demonstrates that TGEV-induced apoptosis is dependent on viral replication in PK-15 cells and occurs through activation of FasL- and mitochondria-mediated apoptotic pathways. 相似文献
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Beyond their nutritional effect, short-chain fatty acids, especially butyrate, modulate cell differentiation, proliferation, motility, and in particular, they induce cell cycle arrest and apoptosis. A bovine kidney epithelial cell line (Madin-Darby bovine kidney; MDBK) was used to investigate the cell cycle regulatory and apoptotic effects of butyrate. Butyrate not only induced apoptosis but also induced cell cycle arrest at the G1/S boundary and M/G2 in MDBK cells (P < 0.01). The cell responses were concentration-dependent (r(2) = 0.9482, P <0.001). In examining possible mechanisms for the apoptosis and cell cycle arrest induced by butyrate, the results showed that butyrate treatment activates caspase-3 activities and induces accumulation of acetylated histone. At least two proteins, cdc6 and cdk1, become targeted for destruction on butyrate treatment. These two proteins are downregulated (P < 0.01 and P < 0.05, respectively) by proteolytic pathways. Moreover, the proteasome inhibitor MG-132 (carbobenzoxy-L-leucyl-L-leucyl-L-leucinal) reverses the cell cycle arrest induced by butyrate, indicating a multiprotein crosstalk wherein the ubiquitination/ proteasome pathway interacted with the caspase-signaling pathway. Because the proteasome inhibitor MG-132 blocked activation of caspase-3, these results functionally locate the proteasome pathway upstream of the caspase pathway. All these results indicate that butyrate functions as both a nutrient and signaling molecule regulating cell growth and proliferation. 相似文献
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Morrison WB 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2012,26(1):18-31
Rudolph Virchow first speculated on a relationship between inflammation and cancer more than 150 years ago. Subsequently, chronic inflammation and associated reactive free radical overload and some types of bacterial, viral, and parasite infections that cause inflammation were recognized as important risk factors for cancer development and account for one in four of all human cancers worldwide. Even viruses that do not directly cause inflammation can cause cancer when they act in conjunction with proinflammatory cofactors or when they initiate or promote cancer via the same signaling pathways utilized in inflammation. Whatever its origin, inflammation in the tumor microenvironment has many cancer-promoting effects and aids in the proliferation and survival of malignant cells and promotes angiogenesis and metastasis. Mediators of inflammation such as cytokines, free radicals, prostaglandins, and growth factors can induce DNA damage in tumor suppressor genes and post-translational modifications of proteins involved in essential cellular processes including apoptosis, DNA repair, and cell cycle checkpoints that can lead to initiation and progression of cancer. 相似文献
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本试验旨在研究HSP60与马立克病肿瘤发生、发展之间的相关性。通过人工感染,建立鸡马立克病肿瘤模型,定期剖杀,利用病理组织学和免疫组织化学方法,检测HSP60与肿瘤细胞定位之间的相关性;设计HSP60 RNA干扰序列,构建重组慢病毒,转染MSB-1细胞,利用流式细胞技术,探索降低HSP60转录表达对MSB-1细胞凋亡水平的影响。结果显示：HSP60在肿瘤细胞的细胞质内强表达;成功构建了HSP60 RNA干扰慢病毒,且5147序列干扰效果最佳;5147序列慢病毒转染48 h时,与对照序列组和空白对照组相比,HSP60转录、表达水平极显著降低（P<0.01）,MSB-1细胞凋亡水平极显著升高（P<0.01）。在马立克病肿瘤发生、发展过程中,HSP60组织细胞定位与肿瘤细胞具有明显的相关性,降低HSP60表达水平能够导致MSB-1细胞凋亡升高,说明HSP60对肿瘤细胞的存活具有重要的生物学作用。 相似文献
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丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)信号通路存在于所有生物体内的大多数细胞内,是哺乳动物细胞重要的信号转导通路,可将细胞表面信号刺激转导至细胞及其核内,与细胞增殖、存活、分化、凋亡等生理病理过程密切相关。在机体发生热应激时,MAPKs信号途径被激活,调控机体产生一系列生物学功能变化。作者综述MAPKs信号转导通路的激活机制和生物效应,重点阐述了MAPKs通路与热应激反应之间的关系。 相似文献
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Bluetongue virus infection: Activation of the MAP kinase-dependent pathway is required for apoptosis
Bluetongue virus (BTV) is a double-stranded RNA virus that induces apoptosis both in mammalian cell cultures and in target tissues. Based on information that members of the mitogen-activated protein kinase family (MAPKs) are mediators of apoptosis, we have examined in detail the MAPK-dependent apoptosis in BTV infection. Previously, we have shown that apoptosis in BTV infection requires the participation of mitochondrial apoptotic pathways. In addition, we demonstrated that NF-κB is activated and that its inhibition substantially reduces cellular apoptosis. For the first time, here we demonstrated the activation of MAPKs after BTV infection. Moreover, by pre-treatment with MAPK inhibitors, c-Jun N-terminal kinases (JNKs) and p38 MAPK, but not extracellular signal-related kinase (ERK), significantly decreased the induction of apoptosis. JNK and p38 activation regulated the cytochrome c released from mitochondria and caspase 3 activation. These results strengthen the understanding of BTV infection and contribute to our previous data confirming that BTV infection induces robust apoptosis in mammalian cells and is likely to play a primary role in BTV pathophysiology. 相似文献
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Buchanan R Popowych Y Dagenais C Arsic N Mutwiri GK Potter AA Babiuk LA Griebel PJ Wilson HL 《Veterinary immunology and immunopathology》2012,145(1-2):453-463
We previously reported that CD21(+) B cells purified from bovine blood do not respond to CpG-ODN stimulation unless either CD14(+) monocytes or B-cell Activating Factor (BAFF), a cytokine produced by activated monocytes, are present. In this report, we present evidence that CD14(+) monocytes are critical for CpG-specific lymphocyte proliferation within the peripheral blood mononuclear cell (PBMC) population but that this response is not mediated by soluble factors produced by CpG-activated monocytes. We further determine that bovine monocytes stimulated with IFN-γ induce expression of the BAFF gene and that recombinant IFN-γ and BAFF induced robust B cell activation when cultured in the absence of CpG ODN. These data suggest that CpG-stimulated monocytes may indirectly promote B cell activation by promoting release of cytokines and/or other soluble factors from accessory cells which in turn act on CpG-stimulated B cells to promote antigen-independent and T cell independent B cell activation. Understanding the T cell independent signals that induce B cell activation has important implications for understanding B cell development in locations where T cells are limited and in understanding polyclonal B cell activation that may contribute to autoimmune diseases. 相似文献