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Min Gu - One of the best experts on this subject based on the ideXlab platform.
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Surface plasmonic gold nanorods for enhanced two-photon microscopic imaging and Apoptosis Induction of cancer cells.
Biomaterials, 2010Co-Authors: Jing Liang Li, Min GuAbstract:Two-photon microscopy powered by a femtosecond laser is a promising tool for luminescence imaging and localized microsurgery of cancers. However, the high energy required to destruct cells limits its medical applications. In this work, gold nanorods were conjugated with transferrin for efficient targeting, two-photon luminescence imaging and enhanced microsurgery of cancer cells. Due to the large two-photon excitation cross section of gold nanorods, gold nanorods are a hundred times more efficient than Fluorescein isothiocyanate (FITC), a common molecular dye, in three-dimensional imaging of cancer cells. The enhanced light absorption and energy conversion by gold nanorods enable treatment of cells with energy fluences two orders of magnitude below that in the absence of gold nanorods. By manipulating the energy fluence, Apoptosis of cancer cells has been achieved. At a same power density, the energy fluence for Apoptosis Induction is less than 20% of that for necrosis. Gold nanorods-enhanced luminescence imaging coupled with Apoptosis Induction of cancer cells provides a medically safe femtosecond laser-based imaging and microsurgery system for cancer diagnosis and treatment.
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Surface plasmonic gold nanorods for enhanced two-photon microscopic imaging and Apoptosis Induction of cancer cells
Biomaterials, 2010Co-Authors: Jing Liang Li, Min GuAbstract:Two-photon microscopy powered by a femtosecond laser is a promising tool for luminescence imaging and localized microsurgery of cancers. However, the high energy required to destruct cells limits its medical applications. In this work, gold nanorods were conjugated with transferrin for efficient targeting, two-photon luminescence imaging and enhanced microsurgery of cancer cells. Due to the large two-photon excitation cross section of gold nanorods, gold nanorods are a hundred times more efficient than Fluorescein isothiocyanate (FITC), a common molecular dye, in three-dimensional imaging of cancer cells. The enhanced light absorption and energy conversion by gold nanorods enable treatment of cells with energy fluences two orders of magnitude below that in the absence of gold nanorods. By manipulating the energy fluence, Apoptosis of cancer cells has been achieved. At a same power density, the energy fluence for Apoptosis Induction is less than 20% of that for necrosis. Gold nanorods-enhanced luminescence imaging coupled with Apoptosis Induction of cancer cells provides a medically safe femtosecond laser-based imaging and microsurgery system for cancer diagnosis and treatment. © 2010 Elsevier Ltd.
Ramida Watanapokasin - One of the best experts on this subject based on the ideXlab platform.
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Antiproliferation and Apoptosis Induction in Colorectal Cancer Cells by Goniothalamin.
Journal of the Medical Association of Thailand = Chotmaihet thangphaet, 2020Co-Authors: Thanet Sophonnithiprasert, Wilawan Mahabusarakam, Yukio Nakamura, Ramida WatanapokasinAbstract:To investigate the effect of goniothalamin on antiproliferation and Apoptosis Induction in three types of colorectal cancer cells. Colorectal cancer is the third of the twentieth most commonly diagnosed cancer. Different types of colorectal cancer cells differ in genotype and characteristics leading to different responses to anticancer drugs. Therefore, finding new anticancer compound for the colorectal cancer cells is necessary. Antiproliferative response of goniothalamin on three colorectal cancer cell lines including Colo 205, SW480, and LoVo were determined by MTT assay. The antiproliferative response at different time and dose was also observed. Apoptosis Induction by goniothalamin was observed in all three cell-lines via morphological changes and nuclear condensation by Hoechst33342 staining. Goniothalamin showed different antiproliferative response on Colo 205, SW480, and Lo Vo cells at the IC50 value is 9.86 ± 0.38 µM, 22.00 ± 4.40 µM, and 65.25 ± 1.85 µM respectively. In addition, the antiproliferative response of goniothalamin was a time- and dose-dependent manner Apoptosis morphological changes and nuclear condensation were clearly observed in Colo 205, SW480 and LoVo cells treated with 10 µM, 25 µM, and 50 µM goniothalamin, respectively. Goniothalamin showed antiproliferation and Apoptosis Induction in colorectal cancer cells with different sensitivity depending on cell type. Investigation of mechanisms underlying Apoptosis and its potential use for colorectal cancer treatment should be further studied.
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Anti-Proliferation and Apoptosis Induction in Breast Cancer Cells by Cratoxylum cochinchinense Extract.
Journal of the Medical Association of Thailand = Chotmaihet thangphaet, 2020Co-Authors: Sukanda Innajak, Wilawan Mahabusarakam, Sirinun Nilwarangoon, Ramida WatanapokasinAbstract:Breast cancer is the most common invasive cancer in females worldwide. It was found about 37.5% in Thai females and is one of the leading causes of death-related cancers in women. Therefore, new finding of anti-cancer compound as a therapeutic candidate in breast cancer is necessary. To investigate the effect of Cratoxylum cochinchinense extract on anti-proliferation and Apoptosis Induction in breast cancer cells. Cell proliferation and cell viability assay were determined by MTT assay. Hoechst 33342 and JC-1 staining were used to determined nuclear morphological changes and mitochondrial membrane potential, respectively. C. cochinchinense extract showed anti-proliferation in MDA-MB-468 treated cells in a time- and dose-dependent manner with IC50 value of 19.19+0.8 μg/ml. In addition, C. cochinchinense extract induced nuclear condensation and apoptotic bodies in MDA-MB-468 treated cells. JC-1 staining revealed that C. cochinchinense extract induced mitochondrial membrane dysfunction. C. cochinchinense extract showed anti-proliferation and Apoptosis Induction properties in MDA-MB-468 treated cells. These results suggested that C. cochinchinense extract may be a potential candidate for anti-cancer drug developing. The underlying mechanisms of Apoptosis Induction should be further studied.
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Mechanism of Apoptosis Induction associated with ERK1/2 upregulation via goniothalamin in melanoma cells
Experimental and Therapeutic Medicine, 2018Co-Authors: Suphakorn Tangchirakhaphan, Sukanda Innajak, Sirinun Nilwarangkoon, Nudjaree Tanjapatkul, Wilawan Mahabusrakum, Ramida WatanapokasinAbstract:The present study aimed to investigate the effect of goniothalamin on Apoptosis Induction in the A375 melanoma cell line. Melanoma is a type of skin cancer with increased prevalence and no potential standard treatment. Goniothalamin is a plant, bioactive styrly-lactone, which has various bioactivities including anti-microbial, anti-inflammatory and anti-cancer. Apoptosis Induction by goniothalamin has been studied in numerous cancer cell lines, however not in the melanoma cell line A375. The results of the MTT assay demonstrated that goniothalamin induced anti-proliferation in a dose dependent manner. Hoechst staining assay demonstrated that goniothalamin induced chromatin condensation and apoptotic bodies in A375 treated cells, and JC-1 staining revealed that goniothalamin induced mitochondrial membrane dysfunction in A375 cells. In addition, goniothalamin decreased the level of anti-apoptotic proteins myeloid cell leukemia 1, B cell lymphoma (Bcl)-2 and Bcl-extra large, whereas it increased the level of pro-apoptotic proteins, Bcl-2 Associated X, Apoptosis regulator, t-BID and Bim in A375 treated cells. In addition, goniothalamin also increased active caspase-9, -7 and cleaved-poly (ADP-ribose) polymerase expression in A375 treated cells. Furthermore, phosphorylated (p)-pyruvate dehydrogenase kinase (PDK) 1 (Ser241) and p-RAC-alpha serine/threonine-protein kinase (Akt; Ser473) were decreased, however c-Jun and p-extracellular signal-regulated kinase (ERK)1/2 were increased upon goniothalamin treatment. These results suggest that goniothalamin has an effect, as anti-proliferation and Apoptosis Induction in A375 cells were associated with upregulated p-ERK1/2, c-Jun and downregulated p-PDK1 (Ser241), p-Akt (Ser473) in A375 cells. Therefore, goniothalamin may be a potential candidate for anti-cancer drug development for melanoma treatment.
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Antiproliferation and Apoptosis Induction in Colorectal Cancer Cells by Goniothalamin.
Journal of the Medical Association of Thailand Chotmaihet thangphaet, 2015Co-Authors: Thanet Sophonnithiprasert, Wilawan Mahabusarakam, Yukio Nakamura, Ramida WatanapokasinAbstract:Objective: To investigate the effect of goniothalamin on antiproliferation and Apoptosis Induction in three types of colorectal cancer cells. Background: Colorectal cancer is the third of the twentieth most commonly diagnosed cancer. Different types of colorectal cancer cells differ in genotype and characteristics leading to different responses to anticancer drugs. Therefore, finding new anticancer compound for the colorectal cancer cells is necessary. Material and Method: Antiproliferative response of goniothalamin on three colorectal cancer cell lines including Colo 205, SW480, and LoVo were determined by MTT assay. The antiproliferative response at different time and dose was also observed. Apoptosis Induction by goniothalamin was observed in all three cell-lines via morphological changes and nuclear condensation by Hoechst33342 staining. Results: Goniothalamin showed different antiproliferative response on Colo 205, SW480, and LoVo cells at the IC50 value is 9.86+0.38 μM, 22.00+4.40 μM, and 65.25+1.85 μM, respectively. In addition, the antiproliferative response of goniothalamin was a time- and dose- dependent manner. Apoptosis morphological changes and nuclear condensation were clearly observed in Colo 205, SW480 and LoVo cells treated with 10 μM, 25 μM, and 50 μM goniothalamin, respectively. Conclusion: Goniothalamin showed antiproliferation and Apoptosis Induction in colorectal cancer cells with different sensitivity depending on cell type. Investigation of mechanisms underlying Apoptosis and its potential use for colorectal cancer treatment should be further studied. Keywords: Colorectal cancer cells, Goniothalamin, Apoptosis, Antiproliferative activity
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Apoptosis Induction associated with the er stress response through up regulation of jnk in hela cells by gambogic acid
BMC Complementary and Alternative Medicine, 2015Co-Authors: Etsu Tashiro, Masaya Imoto, Takahiro Fujimaki, Satoko Shinjo, Aungkana Krajarng, Ramida WatanapokasinAbstract:Background Gambogic acid (GA) was extracted from the dried yellow resin of gamboge (Garcinia hanburyi) which is traditionally used as a coloring material for painting and cloth dying. Gamboge has been also used as a folk medicine for an internal purgative and externally infected wound. We focused on the mechanisms of Apoptosis Induction by GA through the unfold protein response (ER stress) in HeLa cells.
Georg Bauer - One of the best experts on this subject based on the ideXlab platform.
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Nitric oxide mediates Apoptosis Induction selectively in transformed fibroblasts compared to nontransformed fibroblasts
Carcinogenesis, 2020Co-Authors: Stefanie Heigold, Christine Sers, Wibke Bechtel, Boris Ivanovas, Reinhold Schäfer, Georg BauerAbstract:Nitric oxide (NO) mediates Apoptosis Induction in fibroblasts with constitutive src or induced ras oncogene expression, whereas nontransformed parental cells and revertants are not affected. This direct link between the transformed phenotype and sensitivity to NO-mediated Apoptosis Induction seems to be based on the recently described extracellular superoxide anion generation by transformed cells, as NO-mediated Apoptosis Induction in transformed cells is inhibited by extracellular superoxide dismutase (SOD), by SOD mimetics and by apocynin, an inhibitor of NADPH oxidase. Furthermore, nonresponsive nontransformed cells can be rendered sensitive for NOmediated Apoptosis Induction when they are supplemented with xanthine oxidase/xanthine as an extracellular source for superoxide anions. As superoxide anions and NO readily interact in a diffusion-controlled reaction to generate peroxynitrite, peroxynitrite seems to be the responsible Apoptosis inducer in NO-mediated Apoptosis Induction. In line with this conclusion, NO-mediated Apoptosis Induction in superoxide anion-generating transformed cells is inhibited by the peroxynitrite scavengers ebselen and FeTPPS. Moreover, direct application of peroxynitrite induces Apoptosis both in transformed and nontransformed cells, indicating that peroxynitrite is no selective Apoptosis inducer per se, but that selective Apoptosis Induction in transformed cells by NO is achieved through selective peroxynitrite generation. The interaction of NO with target cell derived superoxide anions represents a novel concept for selective Apoptosis Induction in transformed cells. This mechanism may be the basis for selective Apoptosis Induction by natural antitumor systems (like macrophages, natural killer cells, granulocytes) that utilize NO for antitumor action. Apoptosis Induction mediated by NO involves mitochondrial depolarization and is blocked by Bcl-2 overexpression.
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Transformed target cell-derived superoxide anions drive Apoptosis Induction by myeloperoxidase.
Redox Report, 2020Co-Authors: I. Engelmann, S. Dormann, M. Saran, Georg BauerAbstract:Abstract Myeloperoxidase induces Apoptosis in src- or ras-transformed fibroblasts, but not in parental non-transformed fibroblasts. This selectivity seems to be based on superoxide anion production by transformed cells, a recently described characteristic feature of transformed cells. Myeloperoxidase-mediated Apoptosis Induction is inhibited by SOD, catalase, 4-aminobenzoyl hydrazide, taurine and DMSO. This pattern of inhibition allows us to conclude that transformed cell derived superoxide anions dismutate to hydrogen peroxide, which fosters HOCl formation by myeloperoxidase. Hydrogen peroxide formation thereby is the rate-limiting step and depends on the cell density. In a second step, HOCl interacts with superoxide anions to yield the highly reactive Apoptosis inducing hydroxyl radical. This conclusion was verified through selective Apoptosis Induction in transformed cells by direct addition of HOCl, which was also inhibited by SOD and DMSO. Our findings demonstrate a specific interplay between target ...
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Differential Role of Extra- and Intracellular Superoxide Anions for Nitric Oxide-mediated Apoptosis Induction
in Vivo, 2004Co-Authors: Mareike Steinmann, Nicolas Moosmann, Mareike Schimmel, Christina Gerhardus, Georg BauerAbstract:Nitric oxide (NO) has recently been shown to mediate Apoptosis Induction selectively in transformed fibroblasts, in contrast to their nontransformed parental cells. Here we show that NO-mediated Apoptosis Induction in transformed fibroblasts can be divided into two major phases. During phase 1, peroxynitrite is generated by the interaction of extracellular superoxide anions with NO and the intracellular glutathione level is subsequently lowered. This defines the beginning of phase 2, in which NO-mediated signaling depends on intracellular superoxide anions exclusively. The resultant peroxynitrite seems to activate the mitochondrial permeability transition pore and thus triggers execution of Apoptosis. Experimental depletion of intracellular glutathione causes a drastic decrease in the length of phase 1 in transformed cells and renders nontransformed cells sensitive to NO-mediated Apoptosis Induction. These findings allow the prediction that either Induction of superoxide anion generation or glutathione depletion may render cells sensitive to NO-mediated Apoptosis Induction. Nitric oxide (NO) is a free radical with diverse biological functions of central importance (1, for review see ref. 2). It arises from the guanodino group of L-arginine in a NADPH- dependent reaction catalyzed by constitutively expressed or inducible NO synthases (NOS). NO is able to pass cellular membranes (3), to decrease the intracellular glutathione pool (4), to regulate gene expression via interaction with the zinc finger transcription factor SP1 (5) and to up-regulate p53 gene expression (6). The neurotrophic function of NO switches to cell death Induction in midbrain cultures after glutathione depletion (7). Direct Apoptosis Induction by NO has been reported for
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Transformed cell-derived reactive oxygen species support and inhibit nitric oxide-mediated Apoptosis Induction
International Journal of Oncology, 2002Co-Authors: Kathrin Haberstroh, Stefanie Heigold, Georg BauerAbstract:Nitric oxide has been recently shown to require interaction with extracellular superoxide anions and subsequent peroxynitrite formation for selective Apoptosis Induction in transformed fibroblasts. In addition to foster NO-mediated Apoptosis, transformed target cell-derived reactive oxygen species (ROS) also exhibit a marked inhibitory effect directed against NO-mediated Apoptosis. This inhibition can be abrogated by catalase and can be augmented by hydrogen peroxide generation through glucose oxidase. Therefore, transformed fibroblasts at high density seem to inhibit NO-mediated Apoptosis through hydrogen peroxide formation. Inhibition of NO-mediated Apoptosis can be explained by the interaction of hydrogen peroxide with NO, resulting in the generation of hydroxyl radicals. As hydrogen peroxide as well as NO represent far ranging species, hydroxyl radical generation occurs more likely distant from the cell membrane and therefore does not have an Apoptosis-inducing effect on the cells. In total, this reaction is rather blunting Apoptosis Induction mediated by NO. The interaction of hydrogen peroxide with NO may have consequences for the control of transformed cells by NO-utilizing natural antitumor systems.
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Oncogenic transformation increases the sensitivity for Apoptosis Induction by inhibitors of macromolecular synthesis.
International Journal of Oncology, 2000Co-Authors: Hanusch J, Schwieger A, C Sers, R Schäfer, Georg BauerAbstract:Inhibition of RNA or protein synthesis causes Apoptosis in fibroblasts. This points to the constitutive expression of a long-lived Apoptosis machinery which is controlled by shortlived negative regulatory proteins, termed endogenous survival factors. The length of time between addition of the inhibitor of macromolecular synthesis and the onset of Apoptosis can be used as an estimation of the effective survival factor concentration. Transformation of rat fibroblasts by a constitutively expressed src oncogene or an inducible ras oncogene increases the sensitivity for Apoptosis Induction by inhibitors of macromolecular synthesis, indicating that their endogenous survival factor pool has been decreased.
Jing Liang Li - One of the best experts on this subject based on the ideXlab platform.
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Surface plasmonic gold nanorods for enhanced two-photon microscopic imaging and Apoptosis Induction of cancer cells.
Biomaterials, 2010Co-Authors: Jing Liang Li, Min GuAbstract:Two-photon microscopy powered by a femtosecond laser is a promising tool for luminescence imaging and localized microsurgery of cancers. However, the high energy required to destruct cells limits its medical applications. In this work, gold nanorods were conjugated with transferrin for efficient targeting, two-photon luminescence imaging and enhanced microsurgery of cancer cells. Due to the large two-photon excitation cross section of gold nanorods, gold nanorods are a hundred times more efficient than Fluorescein isothiocyanate (FITC), a common molecular dye, in three-dimensional imaging of cancer cells. The enhanced light absorption and energy conversion by gold nanorods enable treatment of cells with energy fluences two orders of magnitude below that in the absence of gold nanorods. By manipulating the energy fluence, Apoptosis of cancer cells has been achieved. At a same power density, the energy fluence for Apoptosis Induction is less than 20% of that for necrosis. Gold nanorods-enhanced luminescence imaging coupled with Apoptosis Induction of cancer cells provides a medically safe femtosecond laser-based imaging and microsurgery system for cancer diagnosis and treatment.
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Surface plasmonic gold nanorods for enhanced two-photon microscopic imaging and Apoptosis Induction of cancer cells
Biomaterials, 2010Co-Authors: Jing Liang Li, Min GuAbstract:Two-photon microscopy powered by a femtosecond laser is a promising tool for luminescence imaging and localized microsurgery of cancers. However, the high energy required to destruct cells limits its medical applications. In this work, gold nanorods were conjugated with transferrin for efficient targeting, two-photon luminescence imaging and enhanced microsurgery of cancer cells. Due to the large two-photon excitation cross section of gold nanorods, gold nanorods are a hundred times more efficient than Fluorescein isothiocyanate (FITC), a common molecular dye, in three-dimensional imaging of cancer cells. The enhanced light absorption and energy conversion by gold nanorods enable treatment of cells with energy fluences two orders of magnitude below that in the absence of gold nanorods. By manipulating the energy fluence, Apoptosis of cancer cells has been achieved. At a same power density, the energy fluence for Apoptosis Induction is less than 20% of that for necrosis. Gold nanorods-enhanced luminescence imaging coupled with Apoptosis Induction of cancer cells provides a medically safe femtosecond laser-based imaging and microsurgery system for cancer diagnosis and treatment. © 2010 Elsevier Ltd.
Hiroo Toyoda - One of the best experts on this subject based on the ideXlab platform.
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Direct contribution of inducible nitric oxide synthase expression to Apoptosis Induction in primary smooth chorion trophoblast cells of human fetal membrane tissues
The International Journal of Biochemistry & Cell Biology, 2008Co-Authors: Bo Yuan, Kunio Ohyama, Makoto Takeichi, Hiroo ToyodaAbstract:We have previously demonstrated that Apoptosis Induction is observed only in smooth chorion laeve trophoblast cells, and not in amnion epithelial cells of human fetal membrane tissues prepared at the term. Apoptosis Induction was suppressed by the presence of an inhibitor specific for inducible nitric oxide synthase (iNOS), suggesting that intracellular oxidative stress plays a critical role in this process. In this study, we transfected the iNOS gene into primary cultured chorion and amnion cells to examine the direct contribution of iNOS gene expression to the Apoptosis Induction in these cells. We identified a significant increase in the levels of iNOS protein expression and nitrite accumulation in both chorion and amnion cells after the iNOS gene transfection. However, the Induction of Apoptosis was observed in an approximately 70% of chorion cells transfected with iNOS gene. Transfection of the iNOS gene into chorion cells resulted in the activation of p38 mitogen-activated protein kinase (MAPK) and downregulation of hemeoxygenase-1 protein expression, whereas no such events were observed in the transfected amnion cells. These results suggest that Apoptosis induced in the chorion trophoblast cells by the iNOS gene expression is closely linked to a physiological consequence, such as the rupture of fetal membranes.
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Imbalance between ROS production and elimination results in Apoptosis Induction in primary smooth chorion trophoblast cells prepared from human fetal membrane tissues.
Life sciences, 2007Co-Authors: Bo Yuan, Kunio Ohyama, Toshio Bessho, Noboru Uchide, Hiroo ToyodaAbstract:We have previously demonstrated that Induction of Apoptosis was observed in the smooth chorion trophoblast cells of human fetal membranes prepared at term, and that Apoptosis progressed rapidly during in vitro incubation of the tissues. Furthermore, we identified the contribution of ROS production system (e.g., oxidant enzymes, such as iNOS and Cox-2) to the Apoptosis Induction in the chorion cells, suggesting an important role of the two inducible enzymes in the Induction process. In this study, we examined the role of ROS elimination system (e.g., antioxidant enzymes, such as glutathione peroxidase (GPx) and catalase) in the Apoptosis Induction of the chorion cells, since the Apoptosis Induction by oxidative stress is a result of imbalance between production and elimination of ROS. Treatment of chorion and amnion cells with mercaptosuccinic acid (MS, GPx inhibitor) and 3-amino-1,2,4-triazole (ATZ, catalase inhibitor) resulted in an inhibition of GPx and catalase activity, respectively. Furthermore, incubation with MS alone induced Apoptosis in the chorion cells and Apoptosis level was enhanced by the addition of ATZ, while ATZ alone hardly induced Apoptosis in the chorion cells. However, none of these reagents induced Apoptosis in the amnion cells. Moreover, an increase of the level of hemeoxygenase-1 gene expression was observed only in the amnion cells when both antioxidant enzyme activities were suppressed. Therefore, we concluded that GPx played a more critical role than catalase in the control of the Apoptosis Induction of the chorion cells, suggesting that the threshold levels of stress tolerance in the chorion cells are much lower than those in the amnion cells.
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Effects of Mitogen-Activated Protein Kinase Inhibitors on Tumor Necrosis Factor-α Gene Expression and Apoptosis Induction in Cultured Human Fetal Membrane Chorion Cells Infected with Influenza Virus
Intervirology, 2006Co-Authors: Noboru Uchide, Kunio Ohyama, Toshio Bessho, Hiroo ToyodaAbstract:Objectives: We investigated the involvement of p38 mitogen-activated protein (MAP) kinase in tumor necrosis factor (TNF)-α gene expression, Apoptosis Induction and virus replication
