Chapter 8 Use of Recombinant Adenovirus for Metabolic Engineering of Mammalian Cells

Becker, Thomas; Noel, Richard J.; Coats, Ward; Gómèz-Foix, Anna M.; Alam, Tausif; Gerard, Robert D.; Newgard, Christopher B.

doi:10.1016/s0091-679x(08)60603-2

Cited by 549 publications

(465 citation statements)

References 71 publications

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“…The recombinant adenovirus expressing GFAT cDNA was generated as described previously [18] by co-transfection of the plasmids pACCMVpLpA-GFAT and pJM17 in 293 cells cultured in DMEM with 7 mmol/l glucose using a calcium phosphate precipitation kit (MBS transfection kit, Stratagene, Heidelberg, Germany).…”

Section: Generation Of Defective Adenovirus Expressing Gfat Cdnamentioning

confidence: 99%

P38 mitogen-activated protein kinase mediates hexosamine-induced TGFβ1 mRNA expression in human mesangial cells

et al. 2003

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Aims/hypothesis. The hexosamine pathway has been implicated in the induction of TGFβ1 expression and in the pathophysiology of diabetic glomerulopathy. Glucose-induced TGFβ1 expression is mediated by p38 mitogen-activated-protein-kinase (p38-MAPK) and this kinase is activated in the diabetic glomeruli. We examined whether the p38-MAPK is implicated in hexosamine-induced TGFβ1 mRNA expression in human mesangial cells. Methods. The products of the hexosamine biosynthetic pathway were increased by the addition of glucosamine or by the overexpression of the rate-limiting enzyme of the hexosamine pathway, glutamine: fructose-6-phosphate amidotransferase (GFAT).Results. Glucosamine addition resulted in cell death. UDP-N-Acetylglucosamine, one of the major hexosamine end-products, was increased in normal (7 mmol/l) and high (25 mmol/l) glucose conditions in GFAT-transfected cells compared to control transfected cells by twofold and 1.7-fold respectively (p≤0.04) and this was accompanied by a 1.6-and 2.3-fold increase (p≤0.02) in TGFβ1 mRNA expression. Addition of the GFAT inhibitor azaserine (10 µmol/l) prevented the induction of TGFβ1 in GFAT transfected cells. GFAT overexpression induced an increase in p38-MAPK activation after 6 and 12 h incubation in normal glucose, and this was prevented by the GFAT inhibitor azaserine. Furthermore, high glucose enhanced p38-MAPK activation in GFAT tranfected cells (p≤0.04). P38-MAPK inhibition using SB202190 (1 µmol/l) reduced hexosamine-induced TGFβ1 expression in normal and high glucose. The activation of the p38-MAPK was dependent on protein kinase-C. Conclusion/interpretation. Overexpression of GFAT increases hexosamine accumulation which mediates TGFβ1 expression via a protein kinase-C and p38-MAPK dependent mechanism. Increased glucose concentrations magnify these effects. [Diabetologia (2003) 46:531-537]

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Section: Generation Of Defective Adenovirus Expressing Gfat Cdnamentioning

confidence: 99%

P38 mitogen-activated protein kinase mediates hexosamine-induced TGFβ1 mRNA expression in human mesangial cells

et al. 2003

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“…Preparation of recombinant replication-deficient adenoviruses All recombinant replication-deficient adenoviruses (type 5) were constructed according to the procedure reported by Becker et al 40 The murine preproendothelin-1 (PPE-1) promoter located upstream to the luciferase gene and the SV40 polyA site, was ligated into the BamHI restriction site of pPAC.plpA (promoterless). The GFP gene was ligated to the PPE-1 promoter into the NotI restriction site.…”

Section: Proliferating and Quiescent Cellsmentioning

confidence: 99%

Tissue-specific gene therapy directed to tumor angiogenesis

et al. 2001

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Gene therapy directed specifically to the vascular wall, particularly to angiogenic endothelial cells is a prerequisite in vascular disease treatment. Angiogenesis is a major feature in many pathological conditions including wound healing, solid tumors, developing metastases, ischemic heart diseases and diabetic retinopathy. In the present study we developed a tissue-specific gene therapy to the angiogenic blood vessels of tumor metastasis using an adeno-based vector containing the murine preproendothelin-1 (PPE-1) promoter. Genes activated by the PPE-1 promoter were highly expressed in bovine aortic endothelial cells in vitro. Systemic injection of the adenoviral vectors AdPPE-1-

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“…29,30 AdTieCH1, AdTieCH2, AdTieCH3 were constructed by replacing the CMV promoter (BglII-PpoI) by a PCR-amplified Tie-1 promoter DNA (866 bp). Individual clones isolated from the initial virus pool were isolated, purified as described 45 and tested for the presence of the promoter and insert DNA by Southern blotting hybridization using a 32 P-labeled L3T4 or Tie-1 promoter cDNA generated by a random-priming kit (Roche Diagnostics, Rotkreuz, Switzerland). Large-scale concentrated stocks were produced from single clones, purified by CsCl gradient centrifugation and titrated by plaque assays.…”

Section: Adtie Constructsmentioning

confidence: 99%

Disruption of integrin-dependent adhesion and survival of endothelial cells by recombinant adenovirus expressing isolated β integrin cytoplasmic domains

Oguey

Rüegg

2000

Gene Ther

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We explored the possibility of using a genetic approach to inhibit integrin-mediated endothelial cell adhesion and survival. We constructed recombinant adenoviruses (Ads) expressing chimeric proteins consisting of the cytoplasmic and transmembrane domains of integrin ␤1 (CH1), ␤3 (CH3) or the ␤1 transmembrane domain alone (CH2) connected to the extracellular domain of L3T4 placed under the control of the CMV promoter (AdCMV) or the endothelial cell specific Tie-1 promoter (AdTie). All constructs were expressed in a dose-and time-dependent manner with over 90% of cells expressing the constructs within 24 h (AdCMVs) or 72 h (AdTies) after infection. Confluent monolayers of HUVEC infected with AdCMVCH1 or AdCMVCH3 detached from the substrate in a time-and dose-dependent manner with over

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Chapter 8 Use of Recombinant Adenovirus for Metabolic Engineering of Mammalian Cells

Cited by 549 publications

References 71 publications

P38 mitogen-activated protein kinase mediates hexosamine-induced TGFβ1 mRNA expression in human mesangial cells

P38 mitogen-activated protein kinase mediates hexosamine-induced TGFβ1 mRNA expression in human mesangial cells

Tissue-specific gene therapy directed to tumor angiogenesis

Disruption of integrin-dependent adhesion and survival of endothelial cells by recombinant adenovirus expressing isolated β integrin cytoplasmic domains

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