The Experts below are selected from a list of 290985 Experts worldwide ranked by ideXlab platform
Jianhua Zhang - One of the best experts on this subject based on the ideXlab platform.
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water stress induced abscisic acid accumulation triggers the Increased Generation of reactive oxygen species and up regulates the activities of antioxidant enzymes in maize leaves
Journal of Experimental Botany, 2002Co-Authors: Mingyi Jiang, Jianhua ZhangAbstract:The interrelationship among water-stress-induced abscisic acid (ABA) accumulation, the Generation of reactive oxygen species (ROS), and the activities of several antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) was investigated in leaves of detached maize (Zea mays L.) plants exposed to -0.7 MPa water stress induced by polyethylene glycol (PEG 6000). Time-course analyses of ABA content, the production of ROS, and the activities of antioxidant enzymes in water-stressed leaves showed that a significant increase in the content of ABA preceded that of ROS, which was followed by a marked increase in the activities of these antioxidant enzymes. Pretreatment with an ABA biosynthesis inhibitor, tungstate, significantly suppressed the accumulation of ABA, and also reduced the Increased Generation of ROS and the up-regulation of these antioxidant enzymes in water-stressed leaves. A mild oxidative stress induced by paraquat, which generates O - 2 and then H 2 O 2 , resulted In a significant enhancement in the activities of antioxidant enzymes in non-water-stressed leaves. Pretreatment with some ROS scavengers, such as Tiron and dimethylthiourea (DMTU), and an inhibitor of NAD(P)H oxidase, diphenyleneiodonium (DPI), almost completely arrested the increase In ROS and the activities of these antioxidant enzymes induced by water stress or ABA treatment. These data suggest that water stress-Induced ABA accumulation triggers the Increased Generation of ROS, which, In turn, leads to the up-regulation of the antioxidant defence system.
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Water stress‐induced abscisic acid accumulation triggers the Increased Generation of reactive oxygen species and up‐regulates the activities of antioxidant enzymes in maize leaves
Journal of experimental botany, 2002Co-Authors: Mingyi Jiang, Jianhua ZhangAbstract:The interrelationship among water-stress-induced abscisic acid (ABA) accumulation, the Generation of reactive oxygen species (ROS), and the activities of several antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) was investigated in leaves of detached maize (Zea mays L.) plants exposed to -0.7 MPa water stress induced by polyethylene glycol (PEG 6000). Time-course analyses of ABA content, the production of ROS, and the activities of antioxidant enzymes in water-stressed leaves showed that a significant increase in the content of ABA preceded that of ROS, which was followed by a marked increase in the activities of these antioxidant enzymes. Pretreatment with an ABA biosynthesis inhibitor, tungstate, significantly suppressed the accumulation of ABA, and also reduced the Increased Generation of ROS and the up-regulation of these antioxidant enzymes in water-stressed leaves. A mild oxidative stress induced by paraquat, which generates O - 2 and then H 2 O 2 , resulted In a significant enhancement in the activities of antioxidant enzymes in non-water-stressed leaves. Pretreatment with some ROS scavengers, such as Tiron and dimethylthiourea (DMTU), and an inhibitor of NAD(P)H oxidase, diphenyleneiodonium (DPI), almost completely arrested the increase In ROS and the activities of these antioxidant enzymes induced by water stress or ABA treatment. These data suggest that water stress-Induced ABA accumulation triggers the Increased Generation of ROS, which, In turn, leads to the up-regulation of the antioxidant defence system.
Pavel Vesely - One of the best experts on this subject based on the ideXlab platform.
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Up-regulation of Rho/ROCK signaling in sarcoma cells drives invasion and Increased Generation of protrusive forces.
Molecular cancer research : MCR, 2008Co-Authors: Daniel Rösel, Jan Brábek, Ondrej Tolde, Claudia Tanja Mierke, Daniel P. Zitterbart, C. Raupach, Krisýtyna Bicanová, Philip Kollmannsberger, Daniela Pankova, Pavel VeselyAbstract:Tumor cell invasion is the most critical step of metastasis. Determination of the mode of invasion within the particular tumor is critical for effective cancer treatment. Protease-independent amoeboid mode of invasion has been described in carcinoma cells and more recently in sarcoma cells on treatment with protease inhibitors. To analyze invasive behavior, we compared highly metastatic sarcoma cells with parental nonmetastatic cells. The metastatic cells exhibited a functional up-regulation of Rho/ROCK signaling and, similarly to carcinoma cells, an amoeboid mode of invasion. Using confocal and traction force microscopy, we showed that an up-regulation of Rho/ROCK signaling leads to Increased cytoskeletal dynamics, myosin light chain localization, and Increased tractions at the leading edge of the cells and that all of these contributed to Increased cell invasiveness in a three-dimensional collagen matrix. We conclude that cells of mesenchymal origin can use the amoeboid nonmesenchymal mode of invasion as their primary invading mechanism and show the dependence of ROCK-mediated amoeboid mode of invasion on the Increased capacity of cells to generate force.
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up regulation of rho rock signaling in sarcoma cells drives invasion and Increased Generation of protrusive forces
Molecular Cancer Research, 2008Co-Authors: Daniel Rösel, Jan Brábek, Ondrej Tolde, Claudia Tanja Mierke, Daniel P. Zitterbart, C. Raupach, Krisýtyna Bicanová, Philip Kollmannsberger, Daniela Pankova, Pavel VeselyAbstract:Tumor cell invasion is the most critical step of metastasis. Determination of the mode of invasion within the particular tumor is critical for effective cancer treatment. Protease-independent amoeboid mode of invasion has been described in carcinoma cells and more recently in sarcoma cells on treatment with protease inhibitors. To analyze invasive behavior, we compared highly metastatic sarcoma cells with parental nonmetastatic cells. The metastatic cells exhibited a functional up-regulation of Rho/ROCK signaling and, similarly to carcinoma cells, an amoeboid mode of invasion. Using confocal and traction force microscopy, we showed that an up-regulation of Rho/ROCK signaling leads to Increased cytoskeletal dynamics, myosin light chain localization, and Increased tractions at the leading edge of the cells and that all of these contributed to Increased cell invasiveness in a three-dimensional collagen matrix. We conclude that cells of mesenchymal origin can use the amoeboid nonmesenchymal mode of invasion as their primary invading mechanism and show the dependence of ROCK-mediated amoeboid mode of invasion on the Increased capacity of cells to generate force.
Mingyi Jiang - One of the best experts on this subject based on the ideXlab platform.
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water stress induced abscisic acid accumulation triggers the Increased Generation of reactive oxygen species and up regulates the activities of antioxidant enzymes in maize leaves
Journal of Experimental Botany, 2002Co-Authors: Mingyi Jiang, Jianhua ZhangAbstract:The interrelationship among water-stress-induced abscisic acid (ABA) accumulation, the Generation of reactive oxygen species (ROS), and the activities of several antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) was investigated in leaves of detached maize (Zea mays L.) plants exposed to -0.7 MPa water stress induced by polyethylene glycol (PEG 6000). Time-course analyses of ABA content, the production of ROS, and the activities of antioxidant enzymes in water-stressed leaves showed that a significant increase in the content of ABA preceded that of ROS, which was followed by a marked increase in the activities of these antioxidant enzymes. Pretreatment with an ABA biosynthesis inhibitor, tungstate, significantly suppressed the accumulation of ABA, and also reduced the Increased Generation of ROS and the up-regulation of these antioxidant enzymes in water-stressed leaves. A mild oxidative stress induced by paraquat, which generates O - 2 and then H 2 O 2 , resulted In a significant enhancement in the activities of antioxidant enzymes in non-water-stressed leaves. Pretreatment with some ROS scavengers, such as Tiron and dimethylthiourea (DMTU), and an inhibitor of NAD(P)H oxidase, diphenyleneiodonium (DPI), almost completely arrested the increase In ROS and the activities of these antioxidant enzymes induced by water stress or ABA treatment. These data suggest that water stress-Induced ABA accumulation triggers the Increased Generation of ROS, which, In turn, leads to the up-regulation of the antioxidant defence system.
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Water stress‐induced abscisic acid accumulation triggers the Increased Generation of reactive oxygen species and up‐regulates the activities of antioxidant enzymes in maize leaves
Journal of experimental botany, 2002Co-Authors: Mingyi Jiang, Jianhua ZhangAbstract:The interrelationship among water-stress-induced abscisic acid (ABA) accumulation, the Generation of reactive oxygen species (ROS), and the activities of several antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) was investigated in leaves of detached maize (Zea mays L.) plants exposed to -0.7 MPa water stress induced by polyethylene glycol (PEG 6000). Time-course analyses of ABA content, the production of ROS, and the activities of antioxidant enzymes in water-stressed leaves showed that a significant increase in the content of ABA preceded that of ROS, which was followed by a marked increase in the activities of these antioxidant enzymes. Pretreatment with an ABA biosynthesis inhibitor, tungstate, significantly suppressed the accumulation of ABA, and also reduced the Increased Generation of ROS and the up-regulation of these antioxidant enzymes in water-stressed leaves. A mild oxidative stress induced by paraquat, which generates O - 2 and then H 2 O 2 , resulted In a significant enhancement in the activities of antioxidant enzymes in non-water-stressed leaves. Pretreatment with some ROS scavengers, such as Tiron and dimethylthiourea (DMTU), and an inhibitor of NAD(P)H oxidase, diphenyleneiodonium (DPI), almost completely arrested the increase In ROS and the activities of these antioxidant enzymes induced by water stress or ABA treatment. These data suggest that water stress-Induced ABA accumulation triggers the Increased Generation of ROS, which, In turn, leads to the up-regulation of the antioxidant defence system.
Daniel Rösel - One of the best experts on this subject based on the ideXlab platform.
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Up-regulation of Rho/ROCK signaling in sarcoma cells drives invasion and Increased Generation of protrusive forces.
Molecular cancer research : MCR, 2008Co-Authors: Daniel Rösel, Jan Brábek, Ondrej Tolde, Claudia Tanja Mierke, Daniel P. Zitterbart, C. Raupach, Krisýtyna Bicanová, Philip Kollmannsberger, Daniela Pankova, Pavel VeselyAbstract:Tumor cell invasion is the most critical step of metastasis. Determination of the mode of invasion within the particular tumor is critical for effective cancer treatment. Protease-independent amoeboid mode of invasion has been described in carcinoma cells and more recently in sarcoma cells on treatment with protease inhibitors. To analyze invasive behavior, we compared highly metastatic sarcoma cells with parental nonmetastatic cells. The metastatic cells exhibited a functional up-regulation of Rho/ROCK signaling and, similarly to carcinoma cells, an amoeboid mode of invasion. Using confocal and traction force microscopy, we showed that an up-regulation of Rho/ROCK signaling leads to Increased cytoskeletal dynamics, myosin light chain localization, and Increased tractions at the leading edge of the cells and that all of these contributed to Increased cell invasiveness in a three-dimensional collagen matrix. We conclude that cells of mesenchymal origin can use the amoeboid nonmesenchymal mode of invasion as their primary invading mechanism and show the dependence of ROCK-mediated amoeboid mode of invasion on the Increased capacity of cells to generate force.
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up regulation of rho rock signaling in sarcoma cells drives invasion and Increased Generation of protrusive forces
Molecular Cancer Research, 2008Co-Authors: Daniel Rösel, Jan Brábek, Ondrej Tolde, Claudia Tanja Mierke, Daniel P. Zitterbart, C. Raupach, Krisýtyna Bicanová, Philip Kollmannsberger, Daniela Pankova, Pavel VeselyAbstract:Tumor cell invasion is the most critical step of metastasis. Determination of the mode of invasion within the particular tumor is critical for effective cancer treatment. Protease-independent amoeboid mode of invasion has been described in carcinoma cells and more recently in sarcoma cells on treatment with protease inhibitors. To analyze invasive behavior, we compared highly metastatic sarcoma cells with parental nonmetastatic cells. The metastatic cells exhibited a functional up-regulation of Rho/ROCK signaling and, similarly to carcinoma cells, an amoeboid mode of invasion. Using confocal and traction force microscopy, we showed that an up-regulation of Rho/ROCK signaling leads to Increased cytoskeletal dynamics, myosin light chain localization, and Increased tractions at the leading edge of the cells and that all of these contributed to Increased cell invasiveness in a three-dimensional collagen matrix. We conclude that cells of mesenchymal origin can use the amoeboid nonmesenchymal mode of invasion as their primary invading mechanism and show the dependence of ROCK-mediated amoeboid mode of invasion on the Increased capacity of cells to generate force.
Michael Papamichail - One of the best experts on this subject based on the ideXlab platform.
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Synergy between interleukin-2 and prothymosin α for the Increased Generation of cytotoxic T lymphocytes against autologous human carcinomas
Cancer immunology immunotherapy : CII, 2000Co-Authors: Ioannis F Voutsas, Constantin N Baxevanis, Angelos D Gritzapis, Ioannis Missitzis, George P. Stathopoulos, George Archodakis, Constantin Banis, Wolfgang Voelter, Michael PapamichailAbstract:Peripheral blood mononuclear cells (PBMC) from cancer patients were cultured in vitro with irradiated autologous tumor cells isolated from malignant effusions (mixed lymphocyte tumor cultures, MLTC) and low-dose (50 IU/ml) recombinant interleukin-2 (IL-2). The combination of IL-2 and prothymosin α (ProTα) resulted in a greater PBMC-induced response to the autologous tumor than that brought about by IL-2 alone. In particular, ProTα specifically enhanced the CD4+ T-cell-mediated proliferation against the autologous tumor. CD4+ T cells seemed to recognize tumor antigens presented by HLA-DR molecules expressed on the autologous monocytes, since preincubation of the latter with an anti-HLA-DR monoclonal antibody (mAb) abrogated the response. In addition, MLTC set up with IL-2 and ProTα also generated more MHC-class-I-restricted cytotoxic T lymphocytes (CTL) against the autologous tumor than did MLTC set up with IL-2 alone. The MLTC-induced CTL contained high levels of cytoplasmic perforin and their development was strictly dependent on the presence of both autologous CD4+ T cells and monocytes. In the absence of either population there was a strong impairment of both proliferative and cytotoxic responses which was not restored by the presence of ProTα. In contrast, when both cell populations were present, ProTα exerted optimal enhancement of CD4+ T cell proliferation, which was associated with potentiated CTL responses. Our data emphasize the role of ProTα for the enhancement of IL-2-induced CTL responses against autologous tumor cells. Such responses require collaborative interactions between CD4+, CD8+ T cells and monocytes as antigen-presenting cells. Our data are relevant for adoptive immunotherapeutic settings utilizing IL-2 and ProTα-induced autologous-tumor-specific CTL.
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Increased Generation of autologous tumor reactive lymphocytes by anti cd3 monoclonal antibody and prothymosin α
Cancer Immunology Immunotherapy, 1999Co-Authors: Constantin N Baxevanis, G Spanakos, Ioannis F Voutsas, Angelos D Gritzapis, Ourania E Tsitsilonis, Avgi Mamalaki, Michael PapamichailAbstract:Anti-CD3 monoclonal antibody (mAb) activates in vitro peripheral blood mononuclear cells (PBMC) to lyse a variety of tumor cell lines in a non-major histocompatibility-complex(MHC)-restricted manner [subsequently referred to as anti-CD3-activated killer (AAK) cytotoxicity]. Prothymosin α (ProTα) is a biological response modifier that exerts its effects primarily on mononuclear cells, especially when these cells' effector functions are impaired. In this study, we report that ProTα enhances the AAK cytotoxicity in PBMC from healthy donors. This effect was more profound with cancer patients' PBMC, which were deficient in their ability to respond with enhanced AAK cytotoxicity upon in vitro stimulation with anti-CD3. Thus, cancer patients' PBMC, activated with a combination of anti-CD3 and ProTα, exhibited Increased AAK activity and efficiently lysed both autologous tumor and Daudi targets. The ProTα effect on PBMC was demonstrated to involve stimulation of adhesion molecules (CD2, CD18, CD54, CD49f) and CD25 expression, up-regulation of perforin mRNA transcription, Increased numbers of perforin-positive (+) cells and elevated production of interleukin-2 (IL-2), interleukin-1β (IL-1β) and tumor necrosis factor α (TNFα). Moreover, effector CD8+ and CD56+ cells pretreated with anti-CD3 and ProTα contained high cytoplasmic perforin levels and Increased expression of IL-1β- and TNFα-specific receptors. The induction of autologous-tumor-reactive CD8+ and CD56+ lymphocytes in anti-CD3-activated PBMC by ProTα provides an alternative protocol aimed at the improvement of clinical results in cellular adoptive immunotherapy of cancer.
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Increased Generation of autologous tumor-reactive lymphocytes by anti-CD3 monoclonal antibody and prothymosin alpha.
Cancer immunology immunotherapy : CII, 1999Co-Authors: Constantin N Baxevanis, G Spanakos, Ioannis F Voutsas, Angelos D Gritzapis, Ourania E Tsitsilonis, Avgi Mamalaki, Michael PapamichailAbstract:Anti-CD3 monoclonal antibody (mAb) activates in vitro peripheral blood mononuclear cells (PBMC) to lyse a variety of tumor cell lines in a non-major histocompatibility-complex(MHC)-restricted manner [subsequently referred to as anti-CD3-activated killer (AAK) cytotoxicity]. Prothymosin alpha (ProTalpha) is a biological response modifier that exerts its effects primarily on mononuclear cells, especially when these cells' effector functions are impaired. In this study, we report that ProTalpha enhances the AAK cytotoxicity in PBMC from healthy donors. This effect was more profound with cancer patients' PBMC, which were deficient in their ability to respond with enhanced AAK cytotoxicity upon in vitro stimulation with anti-CD3. Thus, cancer patients' PBMC, activated with a combination of anti-CD3 and ProTalpha, exhibited Increased AAK activity and efficiently lysed both autologous tumor and Daudi targets. The ProTalpha effect on PBMC was demonstrated to involve stimulation of adhesion molecules (CD2, CD18, CD54, CD49f) and CD25 expression, up-regulation of perforin mRNA transcription, Increased numbers of perforin-positive (+) cells and elevated production of interleukin-2 (IL-2), interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha). Moreover, effector CD8+ and CD56+ cells pretreated with anti-CD3 and ProTalpha contained high cytoplasmic perforin levels and Increased expression of IL-1beta- and TNFalpha-specific receptors. The induction of autologous-tumor-reactive CD8+ and CD56+ lymphocytes in anti-CD3-activated PBMC by ProTalpha provides an alternative protocol aimed at the improvement of clinical results in cellular adoptive immunotherapy of cancer.
