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Ronald G. Crystal - One of the best experts on this subject based on the ideXlab platform.

  • lung overexpression of the vascular endothelial growth factor gene induces pulmonary edema
    American Journal of Respiratory Cell and Molecular Biology, 2000
    Co-Authors: Robert J Kaner, John V Ladetto, Ravi Singh, Norimasa Fukuda, Michael A Matthay, Ronald G. Crystal
    Abstract:

    We hypothesized that the angiogenic mediator, vascular endothelial growth factor (VEGF), known to be expressed in the lung and to be capable of inducing local edema in skin, might evoke the development of lung edema if expressed in excess amounts. To test this hypothesis, we developed an in vivo model of VEGF overexpression in the lung on the basis of delivery to the respiratory epithelium of the VEGF165 complementary DNA by an E1(-) Adenovirus Vector (AdVEGF165). Administration of AdVEGF165 by the intratracheal route (10(9) plaque-forming units [pfu]) to C57Bl/6 mice showed increased expression of VEGF messenger RNA in lung tissue by Northern analysis. Overexpression of VEGF protein in the lung at Days 1 to 10 was confirmed by enzyme-linked immunosorbent assay. Intratracheal administration of AdVEGF165 resulted in a dose-dependent increase in lung wet/dry weight ratios over time, lung histology showed widespread intra- alveolar edema, and pulmonary capillary permeability was significantly increased as quantified by the Evans blue dye assay and [(131)I]albumin permeability. To confirm the specificity of these observations, mice were pretreated with intranasal administration of an Adenovirus Vector expressing a truncated soluble form of the VEGF receptor flt-1 (Adsflt). Adsflt (10(9) pfu) pretreatment completely abrogated the increased lung wet/dry weight ratio caused by AdVEGF165 administration, whereas an identical Adenovirus Vector with an irrelevant transgene had no effect upon subsequent AdVEGF165-induced pulmonary edema. Together, these data suggest that overexpression of VEGF in the lung may be one mechanism of increased pulmonary vascular permeability in the early stages of acute lung injury.

  • Adenovirus Vector mediated perforin expression driven by a glucocorticoid inducible promoter inhibits tumor growth in vivo
    American Journal of Respiratory Cell and Molecular Biology, 1998
    Co-Authors: Ko Narumi, Akira Kojima, Ronald G. Crystal
    Abstract:

    To evaluate the concept that in vivo transfer of perforin complementary DNA (cDNA) will suppress tumor growth, we constructed an Adenovirus Vector (AdGRE.PFP) carrying perforin cDNA driven by the glucocorticoid response element (GRE) promoter. We infected A549 lung carcinoma cells with this Vector in vitro and in vivo, and evaluated cell growth over time. In the presence of dexamethasone, in vitro infection of A549 cells with the AdGRE.PFP Vector yielded perforin messenger RNA (mRNA) transcripts and effectively suppressed A549 cell growth. In accord with these in vitro observations, administration of dexamethasone following direct injection of AdGRE.PFP into established subcutaneous A549 tumors in nude mice resulted in a marked reduction in tumor growth as compared with AdGRE.PFP infection without dexamethasone or with dexamethasone alone. These observations suggest that regulable, Adenovirus-mediated gene expression of perforin cDNA may have potential as a strategy for local control of tumor cell growth.

  • dendritic cells genetically modified with an Adenovirus Vector encoding the cdna for a model antigen induce protective and therapeutic antitumor immunity
    Journal of Experimental Medicine, 1997
    Co-Authors: Wenru Song, Hwailoong Kong, Heather Carpenter, Hideshi Torii, Richard D Granstein, Shahin Rafii, Malcolm A S Moore, Ronald G. Crystal
    Abstract:

    Dendritic cells (DCs) are potent antigen-presenting cells that play a critical role in the initiation of antitumor immune responses. In this study, we show that genetic modifications of a murine epidermis-derived DC line and primary bone marrow–derived DCs to express a model antigen β-galactosidase (βgal) can be achieved through the use of a replication-deficient, recombinant Adenovirus Vector, and that the modified DCs are capable of eliciting antigen-specific, MHC-restricted CTL responses. Importantly, using a murine metastatic lung tumor model with syngeneic colon carcinoma cells expressing βgal, we show that immunization of mice with the genetically modified DC line or bone marrow DCs confers potent protection against a lethal tumor challenge, as well as suppression of preestablished tumors, resulting in a significant survival advantage. We conclude that genetic modification of DCs to express antigens that are also expressed in tumors can lead to antigen-specific, antitumor killer cells, with a concomitant resistance to tumor challenge and a decrease in the size of existing tumors.

  • regional delivery of an Adenovirus Vector containing the escherichia coli cytosine deaminase gene to provide local activation of 5 fluorocytosine to suppress the growth of colon carcinoma metastatic to liver
    Human Gene Therapy, 1996
    Co-Authors: Akihiko Ohwada, Edward A. Hirschowitz, Ronald G. Crystal
    Abstract:

    ABSTRACT To evaluate the hypothesis that regional delivery of an Adenovirus Vector containing the Escherichia coli cytosine deaminase gene (AdCMV.CD) together with systemic 5-FC could suppress the growth of metastatic colon cancer in the liver, the AdCMV.CD Vector was injected 0.8–1 cm from the site of a human colon cancer tumor in the livers of nude mice. The growth of the human colon cancer cells was quantified by dot blot analysis of genomic DNA extracted from tumor-bearing liver, hybridized with a human-specific Alu probe. The combination of regional AdCMV.CD plus systemic 5-fluorocytosine (5-FC) suppressed the growth of the metastatic tumors over the 21 days of evaluation following Vector administration. Histologic evaluation showed necrosis at the site of the tumor in the livers of mice treated with AdCMV.CD/5-FC, but not in control groups. Evaluation of the potential toxicity of AdCMV.CD plus 5-FC on the normal liver showed only mild, self-limited dose-related inflammation, with no deaths. These da...

  • retrograde transfer of replication deficient recombinant Adenovirus Vector in the central nervous system for tracing studies
    Brain Research, 1995
    Co-Authors: Hui Kuo, Ronald G. Crystal, Donald K Ingram, Andrea Mastrangeli
    Abstract:

    Abstract We assessed the application of a replication deficient recombinant Adenovirus Vector as a retrograde tracer in neural pathway studies. The Adenovirus Vector, Ad.RSVBgal, containing the intracellular marker gene, β-galactosidase, was injected directly into the laterodorsal striatum of rats. The retrograde transport of the Vector from the injection site was clearly visible in the cerebral cortex, thalamic nucleus, and substantia nigra. No evidence for anterograde transport of the Vector was found. When the Vector was injected into the genu of the corpus callosum, little uptake of the Vector by fibers was noted which suggested that uptake by fibers-of-passage should not be a problem in tracing studies. The present study demonstrates that adenoviral Vectors can be useful retrograde tracers in the study of afferent connections within the central nervous system.

Kun Chen - One of the best experts on this subject based on the ideXlab platform.

  • Adenovirus Vector expressing mda 7 il 24 selectively induces growth arrests and apoptosis in human hepatocellular carcinoma cell lines independent of the state of p53 gene
    Chinese Journal of Hepatology, 2006
    Co-Authors: Xinbo Xue, Congjun Wang, Jianwei Zheng, Kun Chen
    Abstract:

    OBJECTIVE To investigate the effect of melanoma differentiation associated gene-7/interleukin 24 (MDA/IL-24) on human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and normal liver cell line L02 with a different p53 state. METHODS The MDA-7/IL-24 gene was transfected into human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and hepatocyte line L02 with a replication-incompetent Adenovirus Vector. The mRNA expression of MDA7/IL-24 in HepG2, MHCC97L, Hep3B and L02 cells was confirmed using RT-PCR. Protein expression was confirmed using ELISA assay. MTT assay and flow cytometry were used to study tumor cell proliferation and cell cycle in vitro. Hoechst and flow cytometry assay after annexin-V and PI staining were performed to indicate the apoptosis effect. RESULTS Exogenous MDA-7/IL-24 gene was expressed in HepG2, MHCC97L, Hep3B and L02 cells. The protein product of MDA-7/IL-24 was confirmed in the supernatant. MTT assay and apoptosis test indicated MDA-7/IL-24 could induce growth suppression and apoptosis of HepG2, MHCC97L and Hep3B but could not in L02. Cell cycle test revealed MDA-7/IL-24 could block those cancer cells in G2/M but not in the normal cell L02. CONCLUSION MDA-7/IL-24 selectively induces growth suppression and apoptosis in hepatocellular carcinoma lines HepG2, MHCC97L and Hep3B in vitro independent of the state of p53 gene but not in normal liver cell L02. This indicates MDA-7/IL-24 can be a perfect gene for gene therapy in hepatocellular carcinoma.

  • melanoma differentiation associated gene 7 mda 7 il 24 selectively induces growth suppression apoptosis in human hepatocellular carcinoma cell line hepg2 by replication incompetent Adenovirus Vector
    World Journal of Gastroenterology, 2006
    Co-Authors: Congjun Wang, Xinbo Xue, Kun Chen, Jianwei Zheng, Jian Wang, Jianping Zeng
    Abstract:

    AIM: To investigate the effect of replication-incompetent Adenovirus Vector expressing MDA-7/IL-24 on tumor growth and apoptosis in human hepatocellular carcinoma (HCC) cell line HepG2 and normal liver cell line L02. METHODS: We constructed the recombinant replication-incompetent Ad.mda-7 virus Vector and infected it into the human HCC cell line HepG2 and normal liver cell line L02. RT-PCR was performed to detect the mRNA expressing in cells. by ELISA was used to detect MDA-7/IL-24 protein expression in the culture supernatant. The effect of apoptosis induced by Ad.mda-7 was confirmed by Hoechst staining and flow cytometry assay with Annexin-V and PI staining. MTT assay was used to determine growth inhibition of HepG2 cells, and cell-cycle and hypodiploidy analyses were performed by flow cytometry. RESULTS: Recombinant replication-defective virus expressing MDA-7/IL-24 was constructed successfully. RT-PCR showed that the Ad.mda-7 could mediate the expression of the exogenous gene MDA-7/IL-24 into HepG2 and L02. The concentration of MDA-7/IL-24 protein in supernatant was 130 pg/mL and 110 pg/mL in Ad.mda-7-infected L02 and HepG2 cells, respectively. Ad.mda-7 infection obviously induced apoptosis (from 2.60±0.72% to 33.6±13.2%, P  = 0.00012) and growth suppression in HepG2 (inhibition ratio IR = 68%) and an increase in the percentage of specific cancer cell types at the G2/M phase of the cell cycle (from 6.44% to 32.29%, P < 0.01), but not in L02 cells. CONCLUSION: These results confirm selectively induction of apoptosis and growth suppression by the mda-7/IL-24 gene with replication-incompetent Adenovirus Vector in human hepatocellular carcinoma cell line HepG2.

Xinbo Xue - One of the best experts on this subject based on the ideXlab platform.

  • Adenovirus Vector expressing mda 7 il 24 selectively induces growth arrests and apoptosis in human hepatocellular carcinoma cell lines independent of the state of p53 gene
    Chinese Journal of Hepatology, 2006
    Co-Authors: Xinbo Xue, Congjun Wang, Jianwei Zheng, Kun Chen
    Abstract:

    OBJECTIVE To investigate the effect of melanoma differentiation associated gene-7/interleukin 24 (MDA/IL-24) on human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and normal liver cell line L02 with a different p53 state. METHODS The MDA-7/IL-24 gene was transfected into human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and hepatocyte line L02 with a replication-incompetent Adenovirus Vector. The mRNA expression of MDA7/IL-24 in HepG2, MHCC97L, Hep3B and L02 cells was confirmed using RT-PCR. Protein expression was confirmed using ELISA assay. MTT assay and flow cytometry were used to study tumor cell proliferation and cell cycle in vitro. Hoechst and flow cytometry assay after annexin-V and PI staining were performed to indicate the apoptosis effect. RESULTS Exogenous MDA-7/IL-24 gene was expressed in HepG2, MHCC97L, Hep3B and L02 cells. The protein product of MDA-7/IL-24 was confirmed in the supernatant. MTT assay and apoptosis test indicated MDA-7/IL-24 could induce growth suppression and apoptosis of HepG2, MHCC97L and Hep3B but could not in L02. Cell cycle test revealed MDA-7/IL-24 could block those cancer cells in G2/M but not in the normal cell L02. CONCLUSION MDA-7/IL-24 selectively induces growth suppression and apoptosis in hepatocellular carcinoma lines HepG2, MHCC97L and Hep3B in vitro independent of the state of p53 gene but not in normal liver cell L02. This indicates MDA-7/IL-24 can be a perfect gene for gene therapy in hepatocellular carcinoma.

  • melanoma differentiation associated gene 7 mda 7 il 24 selectively induces growth suppression apoptosis in human hepatocellular carcinoma cell line hepg2 by replication incompetent Adenovirus Vector
    World Journal of Gastroenterology, 2006
    Co-Authors: Congjun Wang, Xinbo Xue, Kun Chen, Jianwei Zheng, Jian Wang, Jianping Zeng
    Abstract:

    AIM: To investigate the effect of replication-incompetent Adenovirus Vector expressing MDA-7/IL-24 on tumor growth and apoptosis in human hepatocellular carcinoma (HCC) cell line HepG2 and normal liver cell line L02. METHODS: We constructed the recombinant replication-incompetent Ad.mda-7 virus Vector and infected it into the human HCC cell line HepG2 and normal liver cell line L02. RT-PCR was performed to detect the mRNA expressing in cells. by ELISA was used to detect MDA-7/IL-24 protein expression in the culture supernatant. The effect of apoptosis induced by Ad.mda-7 was confirmed by Hoechst staining and flow cytometry assay with Annexin-V and PI staining. MTT assay was used to determine growth inhibition of HepG2 cells, and cell-cycle and hypodiploidy analyses were performed by flow cytometry. RESULTS: Recombinant replication-defective virus expressing MDA-7/IL-24 was constructed successfully. RT-PCR showed that the Ad.mda-7 could mediate the expression of the exogenous gene MDA-7/IL-24 into HepG2 and L02. The concentration of MDA-7/IL-24 protein in supernatant was 130 pg/mL and 110 pg/mL in Ad.mda-7-infected L02 and HepG2 cells, respectively. Ad.mda-7 infection obviously induced apoptosis (from 2.60±0.72% to 33.6±13.2%, P  = 0.00012) and growth suppression in HepG2 (inhibition ratio IR = 68%) and an increase in the percentage of specific cancer cell types at the G2/M phase of the cell cycle (from 6.44% to 32.29%, P < 0.01), but not in L02 cells. CONCLUSION: These results confirm selectively induction of apoptosis and growth suppression by the mda-7/IL-24 gene with replication-incompetent Adenovirus Vector in human hepatocellular carcinoma cell line HepG2.

Congjun Wang - One of the best experts on this subject based on the ideXlab platform.

  • Adenovirus Vector expressing mda 7 il 24 selectively induces growth arrests and apoptosis in human hepatocellular carcinoma cell lines independent of the state of p53 gene
    Chinese Journal of Hepatology, 2006
    Co-Authors: Xinbo Xue, Congjun Wang, Jianwei Zheng, Kun Chen
    Abstract:

    OBJECTIVE To investigate the effect of melanoma differentiation associated gene-7/interleukin 24 (MDA/IL-24) on human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and normal liver cell line L02 with a different p53 state. METHODS The MDA-7/IL-24 gene was transfected into human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and hepatocyte line L02 with a replication-incompetent Adenovirus Vector. The mRNA expression of MDA7/IL-24 in HepG2, MHCC97L, Hep3B and L02 cells was confirmed using RT-PCR. Protein expression was confirmed using ELISA assay. MTT assay and flow cytometry were used to study tumor cell proliferation and cell cycle in vitro. Hoechst and flow cytometry assay after annexin-V and PI staining were performed to indicate the apoptosis effect. RESULTS Exogenous MDA-7/IL-24 gene was expressed in HepG2, MHCC97L, Hep3B and L02 cells. The protein product of MDA-7/IL-24 was confirmed in the supernatant. MTT assay and apoptosis test indicated MDA-7/IL-24 could induce growth suppression and apoptosis of HepG2, MHCC97L and Hep3B but could not in L02. Cell cycle test revealed MDA-7/IL-24 could block those cancer cells in G2/M but not in the normal cell L02. CONCLUSION MDA-7/IL-24 selectively induces growth suppression and apoptosis in hepatocellular carcinoma lines HepG2, MHCC97L and Hep3B in vitro independent of the state of p53 gene but not in normal liver cell L02. This indicates MDA-7/IL-24 can be a perfect gene for gene therapy in hepatocellular carcinoma.

  • melanoma differentiation associated gene 7 mda 7 il 24 selectively induces growth suppression apoptosis in human hepatocellular carcinoma cell line hepg2 by replication incompetent Adenovirus Vector
    World Journal of Gastroenterology, 2006
    Co-Authors: Congjun Wang, Xinbo Xue, Kun Chen, Jianwei Zheng, Jian Wang, Jianping Zeng
    Abstract:

    AIM: To investigate the effect of replication-incompetent Adenovirus Vector expressing MDA-7/IL-24 on tumor growth and apoptosis in human hepatocellular carcinoma (HCC) cell line HepG2 and normal liver cell line L02. METHODS: We constructed the recombinant replication-incompetent Ad.mda-7 virus Vector and infected it into the human HCC cell line HepG2 and normal liver cell line L02. RT-PCR was performed to detect the mRNA expressing in cells. by ELISA was used to detect MDA-7/IL-24 protein expression in the culture supernatant. The effect of apoptosis induced by Ad.mda-7 was confirmed by Hoechst staining and flow cytometry assay with Annexin-V and PI staining. MTT assay was used to determine growth inhibition of HepG2 cells, and cell-cycle and hypodiploidy analyses were performed by flow cytometry. RESULTS: Recombinant replication-defective virus expressing MDA-7/IL-24 was constructed successfully. RT-PCR showed that the Ad.mda-7 could mediate the expression of the exogenous gene MDA-7/IL-24 into HepG2 and L02. The concentration of MDA-7/IL-24 protein in supernatant was 130 pg/mL and 110 pg/mL in Ad.mda-7-infected L02 and HepG2 cells, respectively. Ad.mda-7 infection obviously induced apoptosis (from 2.60±0.72% to 33.6±13.2%, P  = 0.00012) and growth suppression in HepG2 (inhibition ratio IR = 68%) and an increase in the percentage of specific cancer cell types at the G2/M phase of the cell cycle (from 6.44% to 32.29%, P < 0.01), but not in L02 cells. CONCLUSION: These results confirm selectively induction of apoptosis and growth suppression by the mda-7/IL-24 gene with replication-incompetent Adenovirus Vector in human hepatocellular carcinoma cell line HepG2.

Jianwei Zheng - One of the best experts on this subject based on the ideXlab platform.

  • Adenovirus Vector expressing mda 7 il 24 selectively induces growth arrests and apoptosis in human hepatocellular carcinoma cell lines independent of the state of p53 gene
    Chinese Journal of Hepatology, 2006
    Co-Authors: Xinbo Xue, Congjun Wang, Jianwei Zheng, Kun Chen
    Abstract:

    OBJECTIVE To investigate the effect of melanoma differentiation associated gene-7/interleukin 24 (MDA/IL-24) on human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and normal liver cell line L02 with a different p53 state. METHODS The MDA-7/IL-24 gene was transfected into human hepatocellular carcinoma cell lines HepG2, MHCC97L and Hep3B and hepatocyte line L02 with a replication-incompetent Adenovirus Vector. The mRNA expression of MDA7/IL-24 in HepG2, MHCC97L, Hep3B and L02 cells was confirmed using RT-PCR. Protein expression was confirmed using ELISA assay. MTT assay and flow cytometry were used to study tumor cell proliferation and cell cycle in vitro. Hoechst and flow cytometry assay after annexin-V and PI staining were performed to indicate the apoptosis effect. RESULTS Exogenous MDA-7/IL-24 gene was expressed in HepG2, MHCC97L, Hep3B and L02 cells. The protein product of MDA-7/IL-24 was confirmed in the supernatant. MTT assay and apoptosis test indicated MDA-7/IL-24 could induce growth suppression and apoptosis of HepG2, MHCC97L and Hep3B but could not in L02. Cell cycle test revealed MDA-7/IL-24 could block those cancer cells in G2/M but not in the normal cell L02. CONCLUSION MDA-7/IL-24 selectively induces growth suppression and apoptosis in hepatocellular carcinoma lines HepG2, MHCC97L and Hep3B in vitro independent of the state of p53 gene but not in normal liver cell L02. This indicates MDA-7/IL-24 can be a perfect gene for gene therapy in hepatocellular carcinoma.

  • melanoma differentiation associated gene 7 mda 7 il 24 selectively induces growth suppression apoptosis in human hepatocellular carcinoma cell line hepg2 by replication incompetent Adenovirus Vector
    World Journal of Gastroenterology, 2006
    Co-Authors: Congjun Wang, Xinbo Xue, Kun Chen, Jianwei Zheng, Jian Wang, Jianping Zeng
    Abstract:

    AIM: To investigate the effect of replication-incompetent Adenovirus Vector expressing MDA-7/IL-24 on tumor growth and apoptosis in human hepatocellular carcinoma (HCC) cell line HepG2 and normal liver cell line L02. METHODS: We constructed the recombinant replication-incompetent Ad.mda-7 virus Vector and infected it into the human HCC cell line HepG2 and normal liver cell line L02. RT-PCR was performed to detect the mRNA expressing in cells. by ELISA was used to detect MDA-7/IL-24 protein expression in the culture supernatant. The effect of apoptosis induced by Ad.mda-7 was confirmed by Hoechst staining and flow cytometry assay with Annexin-V and PI staining. MTT assay was used to determine growth inhibition of HepG2 cells, and cell-cycle and hypodiploidy analyses were performed by flow cytometry. RESULTS: Recombinant replication-defective virus expressing MDA-7/IL-24 was constructed successfully. RT-PCR showed that the Ad.mda-7 could mediate the expression of the exogenous gene MDA-7/IL-24 into HepG2 and L02. The concentration of MDA-7/IL-24 protein in supernatant was 130 pg/mL and 110 pg/mL in Ad.mda-7-infected L02 and HepG2 cells, respectively. Ad.mda-7 infection obviously induced apoptosis (from 2.60±0.72% to 33.6±13.2%, P  = 0.00012) and growth suppression in HepG2 (inhibition ratio IR = 68%) and an increase in the percentage of specific cancer cell types at the G2/M phase of the cell cycle (from 6.44% to 32.29%, P < 0.01), but not in L02 cells. CONCLUSION: These results confirm selectively induction of apoptosis and growth suppression by the mda-7/IL-24 gene with replication-incompetent Adenovirus Vector in human hepatocellular carcinoma cell line HepG2.