ArticleClinical ophthalmology (Auckland, N.Z.)2015
The role of tryptase and anti-type II collagen antibodies in the pathogenesis of idiopathic epiretinal membranes.
Article in Clinical ophthalmology (Auckland, N.Z.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Tryptase and Exogenous Trypsin: Mechanisms and Ophthalmic Applications.Journal of inflammation research · 2023Review
- Possible roles of anti-type II collagen antibody and innate immunity in the development and progression of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Review
- Spontaneous disappearance and recurrence of impending macular hole: a case report.Journal of medical case reports · 2019Article
- Article
- Long-term evaluation of spontaneous release of epiretinal membrane and its possible pathogenesis.Clinical ophthalmology (Auckland, N.Z.) · 2017Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the pathogenesis of idiopathic epiretinal membrane (ERM) from a biochemical perspective, the relationships between ERM and tryptase activity, a serine protease, and the levels of anti-type II collagen (anti-IIC) antibodies in the serum. PATIENTS AND
methodsVitreous samples for measurement of tryptase activity were obtained from 54 eyes of 54 patients who underwent a vitrectomy for vitreoretinal disease, ie, 14 eyes of 14 patients with idiopathic macular hole, 14 eyes of 14 patients with proliferative diabetic retinopathy (PDR), 13 eyes of 13 patients with ERM, and 13 eyes of 13 patients with rhegmatogenous retinal detachment (RRD). Tryptase activity was measured by spectrophotometry. Anti-IIC antibodies were measured in the serum obtained from 17 patients with ERM, eight patients who underwent cataract surgery, 12 patients with PDR, and nine patients with RRD. In these 46 patients, the anti-IIC antibodies were measured using a Human/Monkey Anti-Type I and Type II Collagen IgG Assay Kit.
resultsVitreal tryptase activity (mean ± standard deviation [SD]) in macular hole, PDR, ERM, and RRD was 0.0146±0.0053, 0.0018±0.0018, 0.0166±0.0046, and 0.0117±0.0029 mU/mg protein, respectively. Vitreal tryptase activity was significantly higher in macular hole and ERM than in PDR and RRD (P<0.05, Fisher's protected least significant difference). The serum levels of anti-IIC immunoglobulin G (IgG) antibody (mean ± SD) in ERM, cataract surgery, PDR, and RRD were 58.222±30.986, 34.890±18.165, 55.760±26.008, and 35.453±12.769 units/mL, respectively. The serum levels of anti-IIC IgG antibody were significantly higher in ERM and PDR than in cataract surgery and RRD (P<0.05, Fisher's protected least significant difference, two-sided).
conclusionIn the pathogenesis of ERM, increased vitreal tryptase activity may be involved in tissue fibrosis, and elevated serum anti-IIC antibodies may lead to an immune response at the vitreoretinal interface, thus resulting in membrane formation.
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