Microglia enhanced the angiogenesis, migration and proliferation of co-cultured RMECs

Xinyi Ding1,2,3,4, Ruiping Gu1,2,3,4, Meng Zhang1,2,3,4

  • 1Department of Ophthalmology, Eye and ENT Hospital of Fudan University, 83 Fen Yang Road, Shanghai, 200031, People's Republic of China.

BMC Ophthalmology
|September 19, 2018
PubMed
Abstract

Insights

Activated microglia promote neovascular diseases by increasing vascular endothelial growth factor-A (VEGF-A) and platelet-derived growth factor-BB (PDGF-BB) in retinal microvascular endothelial cells (RMECs). This study clarifies their role in retinal vascular dysfunction.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Immunology

Background:

  • Microglia-mediated inflammation is implicated in neovascular eye diseases like diabetic retinopathy.
  • Activated microglia disrupt the blood-retinal barrier, but the precise mechanisms remain unclear.
  • Understanding microglia's impact on retinal microvascular endothelial cells (RMECs) is crucial.

Purpose of the Study:

  • To investigate whether and how microglia influence the function of retinal microvascular endothelial cells (RMECs).
  • To elucidate the role of microglia in the pathogenesis of retinal neovascular diseases.

Main Methods:

  • Established a Lipopolysaccharides (LPS)-activated microglia model.
  • Co-cultured static or activated microglia with RMECs using a Transwell system.
  • Assessed RMEC function, including angiogenesis, migration, proliferation, and tight junction protein expression.

Main Results:

  • Activated microglia significantly increased vascular endothelial growth factor-A (VEGF-A) and platelet-derived growth factor-BB (PDGF-BB) levels.
  • Co-culture with activated microglia enhanced RMEC angiogenesis, migration, proliferation, and permeability.
  • Microglia altered the phenotype of co-cultured RMECs, impacting vascular function.

Conclusions:

  • Microglia, particularly activated microglia, play a significant role in retinal angiogenesis.
  • Activated microglia are key players in maintaining and disrupting vascular hemostasis in the retinal microvasculature.
  • Further research is needed to fully clarify the underlying mechanisms.

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