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Effects of mTOR inhibition on normal retinal vascular development in the mouse

Rina Yagasaki1, Tsutomu Nakahara1, Asami Mori1

  • 1Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan.

Experimental Eye Research
|December 3, 2014
PubMed

Insights

The mammalian target of rapamycin (mTOR) pathway is crucial for retinal vascular development in mice, with its activity modulated by age. Inhibiting mTOR early in development significantly impacts blood vessel formation.

Area of Science:

  • Ophthalmology
  • Developmental Biology
  • Molecular Biology

Background:

  • Retinal vascular development is a complex process involving endothelial cell proliferation and migration.
  • The mammalian target of rapamycin (mTOR) pathway plays a role in cell growth and is implicated in vascular development.
  • Age-related changes in cellular pathways can influence developmental processes.

Purpose of the Study:

  • To investigate the role of age-related changes in mammalian target of rapamycin (mTOR) activity in endothelial cell growth during mouse retinal vascular development.
  • To compare the effects of mTOR inhibition with vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibition on retinal vascularization.

Main Methods:

  • Mice were treated with the mTOR inhibitor rapamycin at different postnatal ages (P0-P5, P6-P7, P12-P13).
  • The vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 was administered to mice.
  • Retinal vasculature and phosphorylated ribosomal protein S6 (pS6), an indicator of mTOR activity, were assessed using immunohistochemistry.

Main Results:

  • Early rapamycin administration (P0-P5) delayed vascularization and reduced capillary density.
  • Later rapamycin administration (P6-P7, P12-P13) had less pronounced effects on vascular growth and density.
  • KRN633 completely inhibited retinal vascularization when given at P0-P1, with age-dependent reduction in effect.
  • Rapamycin treatment markedly diminished pS6 immunoreactivity in endothelial cells.

Conclusions:

  • The mTOR pathway, activated by VEGF in endothelial cells, contributes to normal retinal vascular development.
  • mTOR pathway activity in endothelial cells is modulated in an age-dependent manner during postnatal development.
  • Targeting the mTOR pathway offers potential for modulating retinal vascular development.
Keywords:
Mammalian target of rapamycinRapamycinRetinaRibosomal protein S6Vascular developmentVascular endothelial growth factor

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