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An Ex Vivo Tissue Culture Model for Fibrovascular Complications in Proliferative Diabetic Retinopathy
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Endothelin-1 is associated with fibrosis in proliferative diabetic retinopathy membranes

William Chang1, Michelle Lajko1, Amani A Fawzi1

  • 1Department of Ophthalmology, Northwestern University, Feinberg School of Medicine, Chicago, IL, United States of America.

Plos One
|January 20, 2018
PubMed
Abstract

Insights

Endothelin-1 and fibrosis are elevated in epiretinal membranes from proliferative diabetic retinopathy. This suggests endothelin-1 may drive endothelial-to-mesenchymal transition in these fibrotic membranes.

Area of Science:

  • Ophthalmology
  • Diabetic Retinopathy
  • Fibrosis Research

Background:

  • Epiretinal membranes (ERMs) are a significant cause of visual impairment in proliferative diabetic retinopathy (PDR).
  • The pathogenesis of ERMs in PDR, particularly the role of fibrosis and cellular transitions, requires further elucidation.

Purpose of the Study:

  • To investigate the relationship between endothelin-1 (ET-1) and fibrosis in ERMs from PDR.
  • To explore the potential involvement of endothelial-to-mesenchymal transition (EndMT) in ERM formation in PDR.

Main Methods:

  • ERMs from PDR and idiopathic ERM cases were analyzed using immunohistochemistry.
  • Markers for ET-1, endothelin receptor B, fibroblasts (S100A4), endothelial cells (CD31), and glial cells were utilized.
  • Confocal laser scanning microscopy and image analysis software quantified ET-1 labeling intensity.

Main Results:

  • ERMs from PDR showed significantly higher ET-1 labeling compared to idiopathic ERMs.
  • Co-localization of ET-1 with CD31 and S100A4 was observed in diabetic ERMs.
  • Diabetic ERMs exhibited increased S100A4-positive cells, indicating heightened fibroblastic activity.

Conclusions:

  • PDR-associated ERMs exhibit elevated ET-1 levels and increased fibroblastic activity.
  • The correlation between ET-1, endothelial, and fibroblastic markers suggests EndMT plays a role in PDR ERM pathogenesis.

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