TY - JOUR T1 - Role of tumour necrosis factor-α (TNFα) in the functional properties of hyalocytes JF - British Journal of Ophthalmology JO - Br J Ophthalmol SP - 261 LP - 265 DO - 10.1136/bjo.2010.190322 VL - 95 IS - 2 AU - Yasuaki Hata AU - Shintaro Nakao AU - Ri-ichiro Kohno AU - Kumiyo Oba AU - Takeshi Kita AU - Muneki Miura AU - Yukio Sassa AU - Alexander Schering AU - Tatsuro Ishibashi Y1 - 2011/02/01 UR - http://bjo.bmj.com/content/95/2/261.abstract N2 - Background/aim Tumour necrosis factor-α (TNFα) is an inflammatory cytokine that is upregulated in various vitreoretinal diseases including uveitis and diabetic retinopathy. Recently, our studies have indicated that hyalocytes contribute to the pathogenesis of these diseases. However, the impact of TNFα on the functional properties of hyalocytes is unknown.Methods Hyalocytes were isolated from bovine eyes. Cellular proliferation, migration and gel contraction in response to TNFα and the other inflammatory cytokines were analysed by thymidine uptake, Boyden's chamber assay and collagen gel contraction assay, respectively. Furthermore, we estimated the effect of dexamethasone on these properties of hyalocytes.Results TNFα promoted proliferation, migration and gel contraction by hyalocytes. Dexamethasone inhibited TNFα-induced proliferation but not migration. Dexamethasone did not inhibit TNFα-induced gel contraction but further increased contraction. Furthermore, dexamethasone inhibited TNFα-induced extracellular signal-related kinase (ERK)1/2 phosphorylation in hyalocytes.Conclusion This study indicates that TNFα in vitreous and retina causes activation of hyalocytes, and the activated hyalocytes contribute to the pathogenesis of inflammatory vitreoretinal diseases. Steroid treatment appears to inhibit the activation of hyalocytes in the early stages of the diseases, but might have adverse effects in the late stage through membrane contraction. ER -