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Tsunehiko Ikeda, Seita Morishita, Masanori Fukumoto, Hiroyuki Suzuki, Teruyo Kida, Hidehiro Oku, Kimitoshi Nakamura, Shingi Takai; The role of tryptase and type II collagen in the pathogenesis of idiopathic epiretinal membranes. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5485.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the pathogenesis of idiopathic epiretinal membrane (ERM) from a biochemical perspective, the relationships between ERMs and the activity of tryptase, a serine protease and the levels of anti-type Ⅱ collagen antibodies (anti-ⅡC antibodies) were investigated.
Vitreous samples for measurement of tryptase activity were obtained from 54 patients (54 eyes) who underwent a vitrectomy for vitreoretinal disease. This included 14 patients (14 eyes) with idiopathic macular hole (MH), 14 patients (14 eyes) with proliferative diabetic retinopathy (PDR), 13 patients (13 eyes) with ERM, and 13 patients (13 eyes) with rhegmatogenous retinal detachment (RRD). Tryptase activity was measured by spectrophotometry. Anti-ⅡC antibodies were measured in serum from 15 patients with ERM and in serum from 10 patients who underwent cataract surgery as controls. Anti-ⅡC antibodies were measured using a human/monkey anti-type type Ⅱ collagen IgG assay kit.
Vitreal tryptase activity (mean ± standard deviation) in MH, 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 MH and ERM (p < 0.05, Fisher’s protected least significant difference). Anti-ⅡC antibody levels were significantly higher in ERM (56.417 ± 35.627 units/mL) than in the control group (30.424 ± 16.128 units/mL) (p=0.042, Mann-Whitney test).
In 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, resulting in membrane formation.
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