Thiazolidinediones reduce pathological neovascularization in ischemic retina via an adiponectin-dependent mechanism

Arterioscler Thromb Vasc Biol. 2010 Jan;30(1):46-53. doi: 10.1161/ATVBAHA.109.198465. Epub 2009 Nov 12.

Abstract

Background- The insulin-sensitizing agents referred to as thiazolidinediones (TZDs) possess antiatherogenic and anti-inflammatory actions that contribute to protection against diabetic macrovascular complications. However, little is known about the effects of TZDs on retinal microvessel disorders.

Objective: To investigate whether TZDs modulate retinal vessel formation in a mouse model of oxygen-induced retinopathy.

Methods and results: Neonatal mice were subjected to ischemia-induced retinopathy to produce pathological neovascular tuft formation. Pioglitazone, 10 mg/kg per day, rosiglitazone, 10 mg/kg per day, or vehicle was given by gavage once a day from postnatal day 7 to postnatal day 17. Systemic treatment of wild-type (WT) mice with TZDs led to a significant decrease in pathological retinal neovascularization during ischemia compared with vehicle treatment, which was accompanied by increased plasma levels of the fat-derived hormone adiponectin (APN). In contrast to WT mice, TZDs had no effects on ischemia-induced pathological retinal vessel formation in APN-knockout (KO) mice. Pioglitazone reduced tumor necrosis factor (TNF) alpha expression in ischemic retina in WT mice but not in APN-KO mice. Furthermore, pioglitazone increased plasma APN levels in TNF-alpha-KO mice but did not affect ischemia-induced pathological retinal neovascularization in this strain.

Conclusions: These data show that TZDs attenuate pathological retinal microvessel formation through APN-mediated modulation of TNF-alpha production.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Adiponectin / blood
  • Adiponectin / genetics
  • Animals
  • Diabetic Retinopathy / drug therapy*
  • Diabetic Retinopathy / metabolism
  • Diabetic Retinopathy / pathology
  • Hypoglycemic Agents / pharmacology*
  • Ischemia / drug therapy
  • Ischemia / metabolism
  • Ischemia / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / metabolism
  • Neovascularization, Pathologic / pathology
  • Pioglitazone
  • Retinal Vessels / drug effects
  • Retinal Vessels / pathology
  • Rosiglitazone
  • Thiazolidinediones / pharmacology*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Adiponectin
  • Adipoq protein, mouse
  • Hypoglycemic Agents
  • Thiazolidinediones
  • Tumor Necrosis Factor-alpha
  • Rosiglitazone
  • AMP-Activated Protein Kinases
  • Pioglitazone