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DsAAV8-mediated gene transfer and beta-cell expression of IL-4 and beta-cell growth factors are capable of reversing early-onset diabetes in NOD mice

Academic Article
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Overview

authors

  • Gaddy, D. F.
  • Riedel, M. J.
  • Bertera, S.
  • Kieffer, T. J.
  • Robbins, Paul D.

publication date

  • August 2012

journal

  • Gene Therapy  Journal

abstract

  • Type-I diabetes is a chronic disease mediated by autoimmune destruction of insulin-producing β-cells. Although progress has been made towards improving diabetes-associated pathologies and the quality of life for those living with diabetes, no therapy has been effective at eliminating disease manifestations or reversing disease progression. Here, we examined whether double-stranded adeno-associated virus serotype 8 (dsAAV8)-mediated gene delivery to endogenous β-cells of interleukin (IL)-4 in combination with β-cell growth factors can reverse early-onset diabetes in NOD mice. Our results demonstrate that a single treatment with dsAAV8 vectors expressing IL-4 in combination with glucagon-like peptide-1 or hepatocyte growth factor/NK1 under the regulation of the insulin promoter enhanced β-cell proliferation and survival in vivo, significantly delaying diabetes progression in NOD mice, and reversing disease in ∼10% of treated NOD mice. These results demonstrate the ability to reverse hyperglycemia in NOD mice with established diabetes by in vivo gene transfer to β-cells of immunomodulatory factors and β-cell growth factors.

subject areas

  • Animals
  • Dependovirus
  • Diabetes Mellitus, Experimental
  • Diabetes Mellitus, Type 1
  • Female
  • Gene Transfer Techniques
  • Genetic Therapy
  • Genetic Vectors
  • Glucagon-Like Peptide 1
  • Hepatocyte Growth Factor
  • Insulin-Secreting Cells
  • Interleukin-4
  • Mice
  • Mice, Inbred NOD
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Research

keywords

  • adeno-associated virus
  • glucagon-like peptide-1
  • hepatocyte growth factor
  • interleukin-4
  • type-I diabetes
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Identity

International Standard Serial Number (ISSN)

  • 0969-7128

Digital Object Identifier (DOI)

  • 10.1038/gt.2011.181

PubMed ID

  • 22089495
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Additional Document Info

start page

  • 791

end page

  • 799

volume

  • 19

issue

  • 8

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