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Adrenal Chromaffin Cell

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Norio Kaneda – One of the best experts on this subject based on the ideXlab platform.

  • establishment and characterization of a noradrenergic Adrenal Chromaffin Cell line tsam5ne immortalized with the temperature sensitive sv40 t antigen
    Cell Biology International, 2011
    Co-Authors: Susumu Kohno, Tomiyasu Murata, Kiyomi Hikita, Naoshi Koide, Norio Kaneda

    Abstract:

    We established a clonal Adrenal medullary Cell line, named tsAM5NE, from transgenic mice harbouring the temperature-sensitive Simian virus 40 large T-antigen gene, under the control of the tyrosine hydroxylase promoter. tsAM5NE Cells conditionally grew at a permissive temperature of 33°C and exhibited the noradrenergic Chromaffin Cell phenotype. To understand the characteristics of tsAM5NE Cells, we first examined the responsiveness of the Cells to ligands of the GDNF (glial Cell line-derived neurotrophic factor) family. tsAM5NE Cells proliferated at the permissive temperature of 33°C in response to either GDNF or neurturin, but not artemin or persephin. At the non-permissive temperature of 39°C, GDNF or neurturin caused tsAM5NE Cells to differentiate into neuron-like Cells; however, the differentiated Cells died in a time-dependent manner. Interestingly, LIF (leukaemia inhibitory factor) did not affect the GDNF-mediated Cell proliferation at 33°C, but promoted the survival and differentiation of GDNF-treated Cells at 39°C. In the presence of GDNF plus LIF, the morphological change induced by the temperature shift was associated with up-regulated expression of neuronal markers, indicating that the Cells had indeed undergone neuronal differentiation. Thus, we demonstrated that tsAM5NE Cells had the capacity to terminally differentiate into neuron-like Cells in response to GDNF plus LIF when the oncogene was inactivated by the temperature shift. Thus, this Cell line provides a useful model system for studying the mechanisms regulating neuronal differentiation.

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  • neuronal differentiation elicited by glial Cell line derived neurotrophic factor and ciliary neurotrophic factor in Adrenal Chromaffin Cell line tsam5d immortalized with temperature sensitive sv40 t antigen
    Journal of Neuroscience Research, 2008
    Co-Authors: Tomiyasu Murata, Masaru Tsuboi, Kiyomi Hikita, Susumu Kohno, Naoshi Koide, Norio Kaneda

    Abstract:

    To understand the characteristics of tsAM5D Cells immortalized with the temperature-sensitive simian virus 40 large T-antigen, we first examined the responsiveness of the Cells to ligands of the glial Cell line-derived neurotrophic factor (GDNF) family. tsAM5D Cells proliferated at the permissive temperature of 33 degrees C in response to either GDNF or neurturin, but not persephin or artemin. At the nonpermissive temperature of 39 degrees C, GDNF or neurturin caused tsAM5D Cells to differentiate into neuron-like Cells; however, the differentiated Cells died in a time-dependent manner. Interestingly, ciliary neurotrophic factor (CNTF) did not affect the GDNF-mediated Cell proliferation at 33 degrees C but promoted the survival and differentiation of GDNF-treated Cells at 39 degrees C. In the presence of GDNF plus CNTF, the morphological change induced by the temperature shift was associated with up-regulated expression of various neuronal marker genes, indicating that the Cells had undergone neuronal differentiation. In addition, tsAM5D Cells caused to differentiate by GDNF plus CNTF at 39 degrees C became dependent solely on nerve growth factor (NGF) for their survival and neurite outgrowth. Moreover, upon treatment with GDNF plus CNTF, the dopaminergic phenotype was suppressed by the temperature shift. Thus, we demonstrated that tsAM5D Cells had the capacity to differentiate terminally into neuron-like Cells in response to GDNF plus CNTF when the oncogene was inactivated by the temperature shift. This Cell line provides a useful model system for studying the role of a variety of signaling molecules for GDNF/CNTF-induced neuronal differentiation.

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  • protective effects of neurotrophic factors on tumor necrosis factor related apoptosis inducing ligand trail mediated apoptosis of murine Adrenal Chromaffin Cell line tsam5d
    Journal of Biological Chemistry, 2006
    Co-Authors: Tomiyasu Murata, Masaru Tsuboi, Kiyomi Hikita, Norio Kaneda

    Abstract:

    Abstract We previously established the murine Adrenal Chromaffin Cell line tsAM5D, which was immortalized with the temperature-sensitive simian virus 40 large T-antigen. tsAM5D Cells have the capacity to differentiate into neuron-like Cells in response to neurotrophic factors when the culture temperature is shifted from 33 to 39 °C. In this model system, the temperature shift in the absence of neurotrophic factors led to Cell death. Hoechst staining analysis revealed that typical apoptotic nuclei appeared in a time-dependent manner after the temperature shift. Upon shifting to 39 °C, the degradation of T-antigen was accompanied by the transcriptional activation of p53 protein. Among the p53 target genes, death receptor 5 (DR5), which is the receptor for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), showed the highest level of induction. Interestingly, TRAIL-neutralizing antibody protected tsAM5D Cells from the temperature shift-induced apoptotic Cell death by blocking the activation of caspase-8 and -3, indicating the involvement of TRAIL-mediated death signaling in the temperature shift-induced apoptosis. Glial Cell line-derived neurotrophic factor (GDNF) inhibited the TRAIL-mediated activation of caspase-8 in tsAM5D Cells exposed to 39 °C and cooperated with basic fibroblast growth factor and ciliary neurotrophic factor. Interestingly, the temperature shift induced oligomerization of DR5, which is the earliest process necessary for transduction of the death signal. This oligomerization was inhibited by treatment with GDNF plus ciliary neurotrophic factor but not by that with GDNF alone or GDNF plus basic fibroblast growth factor. These results are discussed with respect to the intraCellular mechanism underlying the protective function of neurotrophic factors against TRAIL-mediated death signaling.

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Tomiyasu Murata – One of the best experts on this subject based on the ideXlab platform.

  • establishment and characterization of a noradrenergic Adrenal Chromaffin Cell line tsam5ne immortalized with the temperature sensitive sv40 t antigen
    Cell Biology International, 2011
    Co-Authors: Susumu Kohno, Tomiyasu Murata, Kiyomi Hikita, Naoshi Koide, Norio Kaneda

    Abstract:

    We established a clonal Adrenal medullary Cell line, named tsAM5NE, from transgenic mice harbouring the temperature-sensitive Simian virus 40 large T-antigen gene, under the control of the tyrosine hydroxylase promoter. tsAM5NE Cells conditionally grew at a permissive temperature of 33°C and exhibited the noradrenergic Chromaffin Cell phenotype. To understand the characteristics of tsAM5NE Cells, we first examined the responsiveness of the Cells to ligands of the GDNF (glial Cell line-derived neurotrophic factor) family. tsAM5NE Cells proliferated at the permissive temperature of 33°C in response to either GDNF or neurturin, but not artemin or persephin. At the non-permissive temperature of 39°C, GDNF or neurturin caused tsAM5NE Cells to differentiate into neuron-like Cells; however, the differentiated Cells died in a time-dependent manner. Interestingly, LIF (leukaemia inhibitory factor) did not affect the GDNF-mediated Cell proliferation at 33°C, but promoted the survival and differentiation of GDNF-treated Cells at 39°C. In the presence of GDNF plus LIF, the morphological change induced by the temperature shift was associated with up-regulated expression of neuronal markers, indicating that the Cells had indeed undergone neuronal differentiation. Thus, we demonstrated that tsAM5NE Cells had the capacity to terminally differentiate into neuron-like Cells in response to GDNF plus LIF when the oncogene was inactivated by the temperature shift. Thus, this Cell line provides a useful model system for studying the mechanisms regulating neuronal differentiation.

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  • neuronal differentiation elicited by glial Cell line derived neurotrophic factor and ciliary neurotrophic factor in Adrenal Chromaffin Cell line tsam5d immortalized with temperature sensitive sv40 t antigen
    Journal of Neuroscience Research, 2008
    Co-Authors: Tomiyasu Murata, Masaru Tsuboi, Kiyomi Hikita, Susumu Kohno, Naoshi Koide, Norio Kaneda

    Abstract:

    To understand the characteristics of tsAM5D Cells immortalized with the temperature-sensitive simian virus 40 large T-antigen, we first examined the responsiveness of the Cells to ligands of the glial Cell line-derived neurotrophic factor (GDNF) family. tsAM5D Cells proliferated at the permissive temperature of 33 degrees C in response to either GDNF or neurturin, but not persephin or artemin. At the nonpermissive temperature of 39 degrees C, GDNF or neurturin caused tsAM5D Cells to differentiate into neuron-like Cells; however, the differentiated Cells died in a time-dependent manner. Interestingly, ciliary neurotrophic factor (CNTF) did not affect the GDNF-mediated Cell proliferation at 33 degrees C but promoted the survival and differentiation of GDNF-treated Cells at 39 degrees C. In the presence of GDNF plus CNTF, the morphological change induced by the temperature shift was associated with up-regulated expression of various neuronal marker genes, indicating that the Cells had undergone neuronal differentiation. In addition, tsAM5D Cells caused to differentiate by GDNF plus CNTF at 39 degrees C became dependent solely on nerve growth factor (NGF) for their survival and neurite outgrowth. Moreover, upon treatment with GDNF plus CNTF, the dopaminergic phenotype was suppressed by the temperature shift. Thus, we demonstrated that tsAM5D Cells had the capacity to differentiate terminally into neuron-like Cells in response to GDNF plus CNTF when the oncogene was inactivated by the temperature shift. This Cell line provides a useful model system for studying the role of a variety of signaling molecules for GDNF/CNTF-induced neuronal differentiation.

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  • protective effects of neurotrophic factors on tumor necrosis factor related apoptosis inducing ligand trail mediated apoptosis of murine Adrenal Chromaffin Cell line tsam5d
    Journal of Biological Chemistry, 2006
    Co-Authors: Tomiyasu Murata, Masaru Tsuboi, Kiyomi Hikita, Norio Kaneda

    Abstract:

    Abstract We previously established the murine Adrenal Chromaffin Cell line tsAM5D, which was immortalized with the temperature-sensitive simian virus 40 large T-antigen. tsAM5D Cells have the capacity to differentiate into neuron-like Cells in response to neurotrophic factors when the culture temperature is shifted from 33 to 39 °C. In this model system, the temperature shift in the absence of neurotrophic factors led to Cell death. Hoechst staining analysis revealed that typical apoptotic nuclei appeared in a time-dependent manner after the temperature shift. Upon shifting to 39 °C, the degradation of T-antigen was accompanied by the transcriptional activation of p53 protein. Among the p53 target genes, death receptor 5 (DR5), which is the receptor for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), showed the highest level of induction. Interestingly, TRAIL-neutralizing antibody protected tsAM5D Cells from the temperature shift-induced apoptotic Cell death by blocking the activation of caspase-8 and -3, indicating the involvement of TRAIL-mediated death signaling in the temperature shift-induced apoptosis. Glial Cell line-derived neurotrophic factor (GDNF) inhibited the TRAIL-mediated activation of caspase-8 in tsAM5D Cells exposed to 39 °C and cooperated with basic fibroblast growth factor and ciliary neurotrophic factor. Interestingly, the temperature shift induced oligomerization of DR5, which is the earliest process necessary for transduction of the death signal. This oligomerization was inhibited by treatment with GDNF plus ciliary neurotrophic factor but not by that with GDNF alone or GDNF plus basic fibroblast growth factor. These results are discussed with respect to the intraCellular mechanism underlying the protective function of neurotrophic factors against TRAIL-mediated death signaling.

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Kiyomi Hikita – One of the best experts on this subject based on the ideXlab platform.

  • establishment and characterization of a noradrenergic Adrenal Chromaffin Cell line tsam5ne immortalized with the temperature sensitive sv40 t antigen
    Cell Biology International, 2011
    Co-Authors: Susumu Kohno, Tomiyasu Murata, Kiyomi Hikita, Naoshi Koide, Norio Kaneda

    Abstract:

    We established a clonal Adrenal medullary Cell line, named tsAM5NE, from transgenic mice harbouring the temperature-sensitive Simian virus 40 large T-antigen gene, under the control of the tyrosine hydroxylase promoter. tsAM5NE Cells conditionally grew at a permissive temperature of 33°C and exhibited the noradrenergic Chromaffin Cell phenotype. To understand the characteristics of tsAM5NE Cells, we first examined the responsiveness of the Cells to ligands of the GDNF (glial Cell line-derived neurotrophic factor) family. tsAM5NE Cells proliferated at the permissive temperature of 33°C in response to either GDNF or neurturin, but not artemin or persephin. At the non-permissive temperature of 39°C, GDNF or neurturin caused tsAM5NE Cells to differentiate into neuron-like Cells; however, the differentiated Cells died in a time-dependent manner. Interestingly, LIF (leukaemia inhibitory factor) did not affect the GDNF-mediated Cell proliferation at 33°C, but promoted the survival and differentiation of GDNF-treated Cells at 39°C. In the presence of GDNF plus LIF, the morphological change induced by the temperature shift was associated with up-regulated expression of neuronal markers, indicating that the Cells had indeed undergone neuronal differentiation. Thus, we demonstrated that tsAM5NE Cells had the capacity to terminally differentiate into neuron-like Cells in response to GDNF plus LIF when the oncogene was inactivated by the temperature shift. Thus, this Cell line provides a useful model system for studying the mechanisms regulating neuronal differentiation.

    Free Register to Access Article

  • neuronal differentiation elicited by glial Cell line derived neurotrophic factor and ciliary neurotrophic factor in Adrenal Chromaffin Cell line tsam5d immortalized with temperature sensitive sv40 t antigen
    Journal of Neuroscience Research, 2008
    Co-Authors: Tomiyasu Murata, Masaru Tsuboi, Kiyomi Hikita, Susumu Kohno, Naoshi Koide, Norio Kaneda

    Abstract:

    To understand the characteristics of tsAM5D Cells immortalized with the temperature-sensitive simian virus 40 large T-antigen, we first examined the responsiveness of the Cells to ligands of the glial Cell line-derived neurotrophic factor (GDNF) family. tsAM5D Cells proliferated at the permissive temperature of 33 degrees C in response to either GDNF or neurturin, but not persephin or artemin. At the nonpermissive temperature of 39 degrees C, GDNF or neurturin caused tsAM5D Cells to differentiate into neuron-like Cells; however, the differentiated Cells died in a time-dependent manner. Interestingly, ciliary neurotrophic factor (CNTF) did not affect the GDNF-mediated Cell proliferation at 33 degrees C but promoted the survival and differentiation of GDNF-treated Cells at 39 degrees C. In the presence of GDNF plus CNTF, the morphological change induced by the temperature shift was associated with up-regulated expression of various neuronal marker genes, indicating that the Cells had undergone neuronal differentiation. In addition, tsAM5D Cells caused to differentiate by GDNF plus CNTF at 39 degrees C became dependent solely on nerve growth factor (NGF) for their survival and neurite outgrowth. Moreover, upon treatment with GDNF plus CNTF, the dopaminergic phenotype was suppressed by the temperature shift. Thus, we demonstrated that tsAM5D Cells had the capacity to differentiate terminally into neuron-like Cells in response to GDNF plus CNTF when the oncogene was inactivated by the temperature shift. This Cell line provides a useful model system for studying the role of a variety of signaling molecules for GDNF/CNTF-induced neuronal differentiation.

    Free Register to Access Article

  • protective effects of neurotrophic factors on tumor necrosis factor related apoptosis inducing ligand trail mediated apoptosis of murine Adrenal Chromaffin Cell line tsam5d
    Journal of Biological Chemistry, 2006
    Co-Authors: Tomiyasu Murata, Masaru Tsuboi, Kiyomi Hikita, Norio Kaneda

    Abstract:

    Abstract We previously established the murine Adrenal Chromaffin Cell line tsAM5D, which was immortalized with the temperature-sensitive simian virus 40 large T-antigen. tsAM5D Cells have the capacity to differentiate into neuron-like Cells in response to neurotrophic factors when the culture temperature is shifted from 33 to 39 °C. In this model system, the temperature shift in the absence of neurotrophic factors led to Cell death. Hoechst staining analysis revealed that typical apoptotic nuclei appeared in a time-dependent manner after the temperature shift. Upon shifting to 39 °C, the degradation of T-antigen was accompanied by the transcriptional activation of p53 protein. Among the p53 target genes, death receptor 5 (DR5), which is the receptor for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), showed the highest level of induction. Interestingly, TRAIL-neutralizing antibody protected tsAM5D Cells from the temperature shift-induced apoptotic Cell death by blocking the activation of caspase-8 and -3, indicating the involvement of TRAIL-mediated death signaling in the temperature shift-induced apoptosis. Glial Cell line-derived neurotrophic factor (GDNF) inhibited the TRAIL-mediated activation of caspase-8 in tsAM5D Cells exposed to 39 °C and cooperated with basic fibroblast growth factor and ciliary neurotrophic factor. Interestingly, the temperature shift induced oligomerization of DR5, which is the earliest process necessary for transduction of the death signal. This oligomerization was inhibited by treatment with GDNF plus ciliary neurotrophic factor but not by that with GDNF alone or GDNF plus basic fibroblast growth factor. These results are discussed with respect to the intraCellular mechanism underlying the protective function of neurotrophic factors against TRAIL-mediated death signaling.

    Free Register to Access Article