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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
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Modulating vascular intimal hyperplasia using HSV-1 mutant requires activated MEK.

C L Skelly1, Q He, L Spiguel

  • 1Section of Vascular Surgery, Department of Surgery, University of Chicago Medical Center, Chicago, IL 60637, USA. cskelly@surgery.bsd.uchicago.edu

Gene Therapy
|March 16, 2012
PubMed
Summary
This summary is machine-generated.

Genetically engineered herpes simplex virus-1 (HSV-1) effectively treats intimal hyperplasia by targeting smooth muscle cells. This therapy relies on MEK activation, offering a promising approach for cardiovascular procedures.

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Area of Science:

  • Cardiovascular Research
  • Virology
  • Molecular Biology

Background:

  • Cardiovascular procedure outcomes are limited by intimal hyperplasia, a condition driven by pathological smooth muscle cell (SMC) proliferation.
  • Genetically engineered herpes simplex virus (HSV) can inhibit vascular SMC proliferation, but the underlying mechanism remains unclear.
  • The Ras signaling cascade, involving mitogen-activated protein kinase (MAPK) phosphorylation, is implicated in SMC hyperplasia.

Purpose of the Study:

  • To investigate if MAPK kinase (MEK) activity is the molecular mechanism by which mutant HSV prevents SMC hyperplasia.
  • To evaluate the efficacy of a MEK-dependent HSV-1 for treating intimal hyperplasia in vivo.

Main Methods:

  • Utilized genetically engineered herpes simplex-1 viruses (HSV-1) designed to target proliferating SMCs.
  • Assessed the role of MEK activation in mediating the anti-proliferative effects of HSV-1 on SMCs.
  • Demonstrated the therapeutic potential in a clinically relevant in vivo model of intimal hyperplasia.

Main Results:

  • Confirmed that genetically engineered HSV-1 effectively targets proliferating SMCs.
  • Established MEK activation as the molecular basis for HSV-1's anti-proliferative effect on SMCs.
  • Showcased the efficacy and practicality of MEK-dependent HSV-1, with effects modulated by viral dose.

Conclusions:

  • MEK activation is the key mechanism underlying the anti-proliferative action of engineered HSV-1 on SMCs.
  • MEK-dependent HSV-1 demonstrates efficacy in treating intimal hyperplasia in vivo, with dose-dependent control.
  • These findings support the clinical evaluation of genetically engineered HSV-1 for intimal hyperplasia treatment.