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Updated: Mar 14, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
LYSOPHOSPHATIDIC ACIDS AND AUTOTAXIN IN RETINAL VEIN OCCLUSION
Ivanka Dacheva1, Christoph Ullmer, Karolina Ceglowska
1*Department of Ophthalmology, University of Heidelberg, Heidelberg, Germany; †Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland; ‡Department of General Ophthalmology, Medical University of Lublin, Lublin, Poland; §Medical Research Centre, Polish Academy of Science, Warsaw, Poland; ¶Department of Ophthalmology, University of Freiburg, Freiburg, Germany; and **Department of Ophthalmology, University of Southern California, Los Angeles, California.
Purpose:
To analyze the levels of lysophosphatidic acids (LPAs) and autotaxin (ATX) in undiluted vitreous of untreated patients with retinal vein occlusion (RVO).
Methods:
Sixty-four vitreous samples (40 RVO, 24 controls with idiopathic floaters) were analyzed in this retrospective case series using LC/MS for LPAs 16:0, 18:0, 18:1, 20:4, and ELISA kits or Luminex technology for ATX, angiopoetin-1 (ANG-1), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), pigment epithelium-derived factor (PEDF), and vascular endothelial growth factor (VEGF). LPA and ATX levels were correlated with the visual acuity, central macular thickness (CMT), average retinal thickness (AvT), vitreal cytokine levels and with each other.
Results:
Levels of every LPA species tested and ATX were significantly increased in the vitreous fluid from all patients with RVO (total LPAs: 968.0 ± 842.3 nM; ATX: 2.5 ± 1.02 nM) compared with controls (total LPAs: 225.2 ± 292.8 nM, P < 0.0001; ATX: 1.9 ± 1.00 nM, P = 0.005). There were strong positive correlations between the vitreal levels of IL-6, IL-8, MCP-1, VEGF and LPAs.
Conclusion:
Levels of LPAs and ATX were positively correlated with proinflammatory cytokines and VEGF and might thus play an important role in the development of macular edema secondary to RVO.
