Purpose Cyclooxygenases (COX), lipoxygenases (LOX) and cytochrome P450 monooxygenases (CYP) derived eicosanoids have been implicated in ocular surface inflammation and neovascularization. These eicosanoids are subjected to regulation by enzymes such as heme oxygenases (HO) and ferritin. Methods Quantitative PCR and LC-MS/MS based lipidomics were performed on pterygia from patients undergoing surgical pterygium excision. Control tissues consisted of donor corneas. In addition, LC-MS/MS-based lipidomics was performed on tears collected from patients prior to surgery. Results mRNA-expression of HO-2, the constitutive HO isoform, was upregulated by 40 % in pterygia as compared to control tissue, while the mRNA level of the inducible form, HO-1, was downregulated by more than 50 %. Levels of CYP4B1 mRNA showed an approximate 2-fold increase in pterygia compared to control. Lipidomics analysis of tissues indicated a doubling in PGE2 and TxB2 levels in pterygia as compared to control. Among LOX-derived metabolites, the anti-inflammatory 15-HETE levels were significantly reduced in pterygia (79.3±48.11 pg/mg protein) as compared to control (586.2±213.5 pg/mg protein), whereas pro-inflammatory LOX- and CYP4B1-derived 12-HETE levels were 10-fold higher in pterygia (2768±832.3 pg/mg protein) compared to control (231.4±87.35 pg/mg protein). PGE2 and the HETEs were also present in tears from patients with a pterygium, but were not detected in tears from healthy volunteers. Ferritin light and heavy chain mRNA expression levels were 60 % and 30 % lower in pterygia as compared to control. Conclusion We believe a dysfunctional HO-Ferritin system leads to increased levels of proinflammatory mediators, thus contributing to the inflammation characteristic of pterygia.
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