Feedback mechanism between blood vessels and astrocytes in retinal vascular development

Trends Cardiovasc Med. 2009 Feb;19(2):38-43. doi: 10.1016/j.tcm.2009.04.004.

Abstract

To meet tissue requirements for oxygen, blood vessels are efficiently distributed throughout the body. Multiple interactions between the vasculature and surrounding tissues are involved in this process. Retinal vascular development is controlled by interactions between ganglion cells, astrocytes, and endothelial cells. In particular, reciprocal feedback between endothelial cells and astrocytes is crucial for proper vascular patterning. Hypoxia-induced vascular endothelial growth factor expression in astrocytes plays a key role in retinal vascular growth. Recently, leukemia inhibitory factor secreted from endothelial cells was shown to act cooperatively with oxygen as a negative feedback signal. This reciprocal feedback mechanism provides a promising target for novel antiangiogenic strategies against ocular neovascular diseases and cancers. Here, we briefly review what is currently known about the molecular events involved in the cellular interactions between ganglion cells, astrocytes, and endothelial cells that control retinal vascular patterning.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiogenesis Inhibitors / pharmacology
  • Animals
  • Astrocytes / drug effects
  • Astrocytes / metabolism*
  • Cell Communication* / drug effects
  • Cell Hypoxia
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism*
  • Feedback, Physiological
  • Humans
  • Leukemia Inhibitory Factor / metabolism
  • Neovascularization, Physiologic* / drug effects
  • Oxygen / metabolism
  • Retinal Ganglion Cells / metabolism
  • Retinal Neovascularization / metabolism*
  • Retinal Neovascularization / physiopathology
  • Retinal Neovascularization / prevention & control
  • Retinal Vessels / drug effects
  • Retinal Vessels / growth & development
  • Retinal Vessels / metabolism*
  • Signal Transduction* / drug effects
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Angiogenesis Inhibitors
  • Leukemia Inhibitory Factor
  • Vascular Endothelial Growth Factor A
  • Oxygen