• Title, Summary, Keyword: Cell death

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Characterization of Dopaminergic Neuronal Cell Death Induced by either N-Methyl-4-Phenylpyridinium of 6-hydroxydopamine (N-메칠-4-페닐피리디니움 및 6-히드록시도파민으로 유도된 도파민계 신경세포 사멸 기작의 규명)

  • O, Yeong-Jun;Choi, Won-Seok
    • YAKHAK HOEJI
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    • v.41 no.1
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    • pp.86-93
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    • 1997
  • Even though both N-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine have been widely used to establish the experimental model for dopaminergic neuronal ce ll death. mechanisms underlying this phenomenon have not been firmly explored. To investigate how these dopaminergic neurotoxins induce neuronal cell death, murine dopaminergic neuronal cell line, MN9D cells were treated with various concentration of either 6-hydroxydopamine or active form of MPTP, N methyl-4-phenylpyridinium (MPP$^+$). Treatment of cells with 5-100 uM 6-hydroxydopamine resulted in apoptotic cell death whereas cell death induced by 5~50 uM MPP$^+$ was not demonstrated typical apoptotic characteristics such as cell shrinkage, apoptotic body and nuclear condensation. Cell death induced by 6-hydroxydopamine was partially blocked in the presence of antioxidants including soluble form of vitamin E or desferrioxamine suggesting that generation of oxidative stress may be associated with 6-hydroxydopamine-induced cell death in MN9D cells. In contrast, MPP$^+$-induced cell death was not blocked by treatment with any of antioxidants tested. As previously demonstrated that MPP$^+$ caused metabolic alterations such as glucose metabolism, removal of glucose from the medium partially inhibited MPP$^+$-induced cell death suggesting excessive cycles of glycolysis may be associated with MPP$^+$-induced cell death. Taken together, these studies demonstrate that two types of dopaminergic neurotoxins recruit distinct neuronal cell death pathways.

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Ceramide Induces Cell Death through an ERK-dependent Mitochondrial Apoptotic Pathway in Renal Epithelial Cells

  • Jung, Soon-Hee
    • Korean Journal of Clinical Laboratory Science
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    • v.42 no.1
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    • pp.46-54
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    • 2010
  • Ceramide induces cell death in a variety of cell types however, the underlying molecular mechanisms related to renal epithelial cells remain unclear. The present study was undertaken to determine the role of extracellular signal-regulated protein kinase (ERK) in ceramide-induced cell death in renal epithelial cells. An established renal proximal tubular cell line of opossum kidney (OK) cells was used for this research. Ceramide induced apoptotic cell death in these cells. Western blot analysis showed that ceramide induced activation of ERK. The ERK activation and cell death induced by ceramide were prevented by the ERK inhibitor PD98059. Ceramide caused cytochrome C release from mitochondria into the cytosol as well as activation of caspase-3. Both effects were prevented by PD98059. The ceramide-induced cell death was also prevented by a caspase inhibitor. These results suggest that ceramide induces cell death through an ERK-dependent mitochondrial apoptotic pathway in OK cells.

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The Hypersensitive Response. A Cell Death during Disease Resistance

  • Park, Jeong-Mee
    • The Plant Pathology Journal
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    • v.21 no.2
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    • pp.99-101
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    • 2005
  • Host cell death occurs during many, but not all, interactions between plants and the pathogens that infect them. This cell death can be associated with disease resistance or susceptibility, depending on the nature of the pathogen. The most well-known cell death response in plants is the hypersensitive response (HR) associated with a resistance response. HR is commonly regulated by direct or indirect interactions between avirulence proteins from pathogen and resistance proteins from plant and it can be the result of multiple signaling pathways. Ion fluxes and the generation of reactive oxygen species commonly precede cell death, but a direct involvement of the latter seems to vary with the plant-pathogen combination. Exciting advances have been made in the identification of cellular protective components and cell death suppressors that might operate in HR. In this review, recent progress in the mechanisms by which plant programmed cell death (PCD) occurs during disease resistance will be discussed.

A Correlative Study on Amyloid β-Induced Cell Death Independent of Caspase Activation

  • Tuyet, Pham Thi Dieu
    • Journal of the Chosun Natural Science
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    • v.7 no.2
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    • pp.87-91
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    • 2014
  • Amyloid beta ($A{\beta}$) peptide has been implicated in the pathogenesis of Alzheimer's disease and has been reported to induce apoptotic death in cell culture. Cysteine Proteases, a family of enzymes known as caspases, mediate cell death in many models of apoptosis. In the present study, we examined the caspase activity and cell death in $A{\beta}$-treated SHSY5Y cells, as an attempt to elucidate the relationship between the type of caspase and $A{\beta}$-induced cell death. $A{\beta}$ at 20 ${\mu}M$ induce activation of caspase-3, 8 and 9 activity, but not the caspase-1. Caspase-3, 8 and 9 were processed by Ab treatment, consistent with the activity assay. Inhibition of the caspase activities by the selective inhibitors, however, marginally affected the cell death induced by $A{\beta}$. Taken together, the results indicate that $A{\beta}$-induced cell death may be independent of caspase activity and rather, the enzymes might be activated as a result of the cell death.

Effect of Zinc on Vascular Smooth Muscle Cell Death Mediated by PDTC

  • Moon Sung-Kwon;Ha Sang-Do
    • Biotechnology and Bioprocess Engineering:BBE
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    • v.5 no.1
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    • pp.40-43
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    • 2000
  • Pyrrolidinedithiocarbamate (PDTC) and N-Acetylcysteine (NAC) are metal and nonmetal-chelating antioxidant which can induce rat and human smooth muscle cell death. When the smooth muscle cells from mouse aorta (MASMC) that we successfully cultured recently was exposed to PDTC and NAC in a normal serum state, the cells were induced to death by these compounds. However, PDTC did not induce the cell death in a serum depleted medium. This data suggests that certain factors in the serum may mediate the cytotoxic effect of PDTC. The metal chelator, Ca-EDTA blocked PDTC-induced cell death, but Cu-, Fe-, and Zn-EDTA did not block the PDTC-induced cell death. This data indicated that copper, iron, and zinc in the serum may lead to the cytotoxic effect of PDTC. Investigation of the intracellular zinc level in PDTC-induced smooth muscle cell death using the zinc probe dye N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide shows that only the muscle-containing layers of the arteries have higher level of zinc. As expected, PDTC increased the intracellular fluorescence level of the zinc. In agreement with these results, the addition of an exogenous metal, zinc, induced the vascular aortic smooth muscle cell death which led to an increased intracellular zinc level. We concluded that PDTC induced mouse aortic smooth muscle cell death required not only zinc level but also intracellular copper and iron level. The mechanism of this antioxidant to induce vascular smooth muscle cell death may provide a new strategy to prevent their proliferation in arteriosclerotic lesions.

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Similarities of Tobacco Mosaic Virus-Induced Hypersensitive Cell Death and Copper-Induced Abiotic Cell Death in Tobacco

  • Oh, Sang-Keun;Cheong, Jong-Joo;Ingyu Hwang;Park, Doil
    • The Plant Pathology Journal
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    • v.15 no.1
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    • pp.8-13
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    • 1999
  • Hypersensitive cell death of plants during incompatible plant-pathogen interactions is one of the efficient defense mechanisms of plants against pathogen infections. For better understanding of the molecular mechanisms involved in the plant hypersensitive response (HR), TMV-induced biotic plant cell death and CuSO4-induced abiotic plant cell death were compared in terms of expression patterns of ten different defense-related genes as molecular markers. The genes include five pathogenesis-related protein genes, two plant secondary metabolite-associated genes, two oxidative stress-related genes and one wound-inducible gene isolated from tobacco. Northern blot analyses revealed that a same set of defense-related genes was induced during both biotic and abiotic cell death but with different time and magnitude. The expression of defense-related genes in tobacco plants was temporarily coincided with the time of cell death. However, when suspension cell cultures was used to monitor the expression of defense-related genes, different patterns of the gene expression were detected. This result implies that three are common and, in addition, also different branches of signaling pathways leading to the induced expression of defense-related genes in tobacco during the pathogen- and heavy metal-induced cell death.

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Programmed Cell death in plants

  • Fukuda, Hiroo
    • Proceedings of the Botanical Society of Korea Conference
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    • pp.69-73
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    • 1999
  • In plants as well as in other multicellular organisms, programmed cell death plays essential roles in the abortion or formation of specific cells and tissues during development to organize the plant [11, 15, 18]. A typical example of developmentally programmed cell death in plants is the death during differentiation of tracheary elements which are components of vessels and tracheids, a water-conducting system. The programming of cell death during tracheary element differentiation has been revealed to be unique to plant cells by using the in vitro Zinnia mesophyll cell culture system. In particular, new biosynthesis of autolysis-related enzymes such as cysteine proteases and nucleases, their accumulation of the vacuole and the programmed collapse of the vacuole are essential to the death of tracheary elements and differ greatly from the process of the apoptotic cell death in animals.

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Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

  • Kim, Kyeong Ah;Kim, Ju Young;Lee, Young Ah;Min, Arim;Bahk, Young Yil;Shin, Myeong Heon
    • The Korean Journal of Parasitology
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    • v.51 no.1
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    • pp.61-68
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    • 2013
  • Entamoeba histolytica, which causes amoebic colitis and occasionally liver abscess in humans, is able to induce host cell death. However, signaling mechanisms of colon cell death induced by E. histolytica are not fully elucidated. In this study, we investigated the signaling role of NOX in cell death of HT29 colonic epithelial cells induced by E. histolytica. Incubation of HT29 cells with amoebic trophozoites resulted in DNA fragmentation that is a hallmark of apoptotic cell death. In addition, E. histolytica generate intracellular reactive oxygen species (ROS) in a contact-dependent manner. Inhibition of intracellular ROS level with treatment with DPI, an inhibitor of NADPH oxidases (NOXs), decreased Entamoebainduced ROS generation and cell death in HT29 cells. However, pan-caspase inhibitor did not affect E. histolytica-induced HT29 cell death. In HT29 cells, catalytic subunit NOX1 and regulatory subunit Rac1 for NOX1 activation were highly expressed. We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Suppression of Rac1 by siRNA significantly inhibited Entamoeba-induced cell death. Moreover, knockdown of NOX1 by siRNA, effectively inhibited E. histolytica-triggered DNA fragmentation in HT29 cells. These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica.

Monosiphonous growth and cell-death in an unusual Bostrychia (Rhodomelaceae, Rhodophyta): B. anomala sp. nov.

  • West, John A.;Loiseaux de Goer, Susan;Zuccarello, Giuseppe C.
    • ALGAE
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    • v.28 no.2
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    • pp.161-171
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    • 2013
  • A morphologically distinct lineage within the Bostrychia moritziana-B. radicans species complex is described as a new species. Bostrychia anomala has thalli with branched monosiphonous filaments with apical cell divisions. The species has terminal tetrasporangial stichidia, each subtending cell bearing tetrasporangia with 2 cover cells. Discharged spores divide transversely, the lower cell first forming a narrow rhizoid and the upper cell forming a monosiphonous shoot. Females have subterminal procarps and males have terminal spermatangial stichidia. Carposporophytes are spherical. Isolates in culture show a pattern of cell death not associated with injury, reminiscent of programmed cell death. Bostrychia anomola shows cell death at intervals along the filaments resulting in division of adjacent cells on either side of the dead cell re-joining the filament; cell division of only one adjacent cell resulting in branching at that site; or filaments fragmenting at the cell death point with adjacent cells forming new apical cells, a means of thallus propagation. The cell death pattern could be a method of filament propagation in the mangrove environment where sexual reproduction is rare.

Novel non-apoptotic cell death: ferroptosis (새로운 non-apoptotic 세포사멸: ferroptosis)

  • Woo, Seon Min;Kwon, Taeg Kyu
    • Yeungnam University Journal of Medicine
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    • v.34 no.2
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    • pp.174-181
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    • 2017
  • Ferroptosis is a newly recognized type of cell death that results from iron-dependent lipid peroxidation and is different from other types of cell death, such as apoptosis, necrosis, and autophagic cell death. This type of cell death is characterized by mitochondrial shrinkage with an increased mitochondrial membrane density and outer mitochondrial membrane rupture. Ferroptosis can be induced by a loss of activity of system $X_c{^-}$ and the inhibition of glutathione peroxidase 4, followed by the accumulation of lipid reactive oxygen species (ROS). In addition, inactivation of the mevalonate and transsulfuration pathways is involved in the induction of ferroptosis. Moreover, nicotinamide adenine dinucleotide phosphate oxidase and p53 promote ferroptosis by increasing ROS production, while heat shock protein beta-1 and nuclear factor erythroid 2-related factor 2 inhibit ferroptosis by reducing iron uptake. This article outlines the molecular mechanisms and signaling pathways of ferroptosis regulation, and explains the roles of ferroptosis in human disease.