Construction of adenoviral and retroviral vectors coexpressing the genes encoding the hepatitis B surface antigen and B7-1 protein

He, Xiaosong; Rivkina, Marianne; Robinson, William S.

doi:10.1016/0378-1119(96)00136-9

Cited by 15 publications

(9 citation statements)

References 20 publications

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“…Adenoviral vectors were constructed as described by He et al (19). One hour following isolation, cardiomyocytes were transfected by the different adenovirus (MOI 50) for at least 36 h before treatment with serotonin.…”

Section: Adenoviral Vector Infectionmentioning

confidence: 99%

A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor‐independent ROS generation

et al. 2005

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Reactive oxygen species (ROS) play a critical role in cardiac hypertrophy. We have recently shown that the serotonin-degrading enzyme monoamine oxidase A (MAO A) is an important source of hydrogen peroxide in rat heart. In the present study, we investigated the potential role of hydrogen peroxide generated by MAO A in cardiomyocyte hypertrophy by serotonin. Serotonin (5 microM, 48 h) induced hypertrophy in cultured adult rat ventricular myocytes, as reflected by increased 3H-leucine incorporation (+43%, P<0.001) and total protein content (+22%, P<0.001). Serotonin also increased intracellular hydrogen peroxide and oxidative stress production, measured respectively by DCF fluorescence intensity and GSH/GSSG ratio, and promoted ERK1/2 phosphorylation (P<0.001). Serotonin effects were only partially inhibited by the 5-HT2B receptor antagonist SB 206553. In contrast, they were extensively (>80%) prevented by the amine uptake inhibitor imipramine, the MAO inhibitor pargyline and the MEK inhibitor PD 98059. Cardiomyocyte hypertrophy and ERK activation were also inhibited by decreasing intracellular ROS by adenoviral overexpression of catalase or cardiomyocytes treatment with the iron chelator deferoxamine. These data suggest that part of cardiac hypertrophic effect of serotonin requires hydrogen peroxide production by MAO A and ERK1/2 activation. This newly recognized, receptor-independent mechanism of serotonin may contribute to myocardial remodeling and failure.

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Section: Adenoviral Vector Infectionmentioning

confidence: 99%

A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor‐independent ROS generation

et al. 2005

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“…The recombinant adenoviruses encoding the wild-type and mutant p38␣ were produced according to the method of He et al (19) with some modifications. Briefly, the FLAG-tagged wild-type and mutant human p38␣ cDNAs were cloned into the shuttle vector pAdTrack-CMV, linearized, and cotransformed into Escherichia coli BJ5183 cells along with the adenoviral backbone vector pAdEasy-1.…”

Section: Reagents and Plasmidsmentioning

confidence: 99%

IL-6 activates serum and glucocorticoid kinase via p38α mitogen-activated protein kinase pathway

Meng¹,

Yamagiwa²,

Taffetani³

et al. 2005

American Journal of Physiology-Cell Physiology

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“…Viral gene transfer has been shown to be highly efficient in numerous preclinical and clinical experiments. Modified recombinant viral gene vectors such as vaccinia-, retro-, herpes simplex and adenovirus have been demonstrated to be powerful tools for gene transfer [63,94,[134][135][136]. The majority of clinical trials have utilised murine retroviral vectors due to the lack of homology with human retroviruses [137].…”

Section: Carrier Mediated Transfection Systemsmentioning

confidence: 99%

DNA‐based immunotherapy: potential for treatment of chronic viral hepatitis?

Beckebaum

Cicinnati

Gerken

2002

Reviews in Medical Virology

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Persistent HBV and HCV infection represent major causes of chronic liver disease with a high risk of progression to liver cirrhosis and hepatocellular carcinoma (HCC). Conventional protein-based vaccines are highly efficacious in preventing HBV infection; whereas in therapeutic settings with chronically infected patients, results have been disappointing. Prophylactic vaccination against HCV infection has not yet been achieved due to many impediments including frequent spontaneous mutations of the virus with escape from immune system control. Using animal models it has been demonstrated that DNA-based immunisation strategies may overcome this problem because of their potential to induce immunity against multiple viral epitopes. DNA-based vaccines mimic the effect of live attenuated viral vaccines, eliciting cell mediated immunity in addition to inducing humoral responses. Efficacy may further be improved by addition of DNA encoding immunomodulatory cytokines and more recently, direct genetic modulation of antigen-presenting cells, such as dendritic cells (DC), has been shown to increase antigen-specific immune responses. This review focuses on immunological aspects of chronic HBV and HCV infection and on the potential of DNA- and DC-based vaccines for the treatment of chronic viral hepatitis.

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Construction of adenoviral and retroviral vectors coexpressing the genes encoding the hepatitis B surface antigen and B7-1 protein

Cited by 15 publications

References 20 publications

A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor‐independent ROS generation

A new hypertrophic mechanism of serotonin in cardiac myocytes: receptor‐independent ROS generation

IL-6 activates serum and glucocorticoid kinase via p38α mitogen-activated protein kinase pathway

DNA‐based immunotherapy: potential for treatment of chronic viral hepatitis?

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