Local anti-angiogenic therapy by magnet-assisted downregulation of SHP2 phosphatase

J Control Release. 2019 Jul 10:305:155-164. doi: 10.1016/j.jconrel.2019.05.031. Epub 2019 May 21.

Abstract

Anti-angiogenic therapies are promising options for diseases with enhanced vessel formation such as tumors or retinopathies. In most cases, a site-specific local effect on vessel growth is required, while the current focus on systemic distribution of angiogenesis inhibitors may cause severe unwanted side-effects. Therefore, in the current study we have developed an approach for the local inhibition of vascularization, using complexes of lentivirus and magnetic nanoparticles in combination with magnetic fields. Using this strategy in the murine embryonic stem cell (ESC) system, we were able to site-specifically downregulate the protein tyrosine phosphatase SHP2 by RNAi technology in areas with active vessel formation. This resulted in a reduction of vessel development, as shown by reduced vascular tube length, branching points and vascular loops. The anti-angiogenic effect could also be recapitulated in the dorsal skinfold chamber of mice in vivo. Here, site-specific downregulation of SHP2 reduced re-vascularization after wound induction. Thus, we have developed a magnet-assisted, RNAi-based strategy for the efficient local inhibition of angiogenesis in ESCs in vitro and also in vivo.

Keywords: Anti-angiogenesis; Embryonic stem cells; Gene therapy; Lentivirus; Magnetic nanoparticles.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Down-Regulation*
  • Genetic Vectors / administration & dosage
  • Genetic Vectors / genetics*
  • Lentivirus / genetics*
  • Magnets / chemistry
  • Mice
  • Mouse Embryonic Stem Cells / metabolism*
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / therapy
  • Neovascularization, Physiologic*
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics*
  • RNA Interference
  • Transduction, Genetic / methods

Substances

  • Protein Tyrosine Phosphatase, Non-Receptor Type 11