Role of tumour necrosis factor-α (TNFα) in the functional properties of hyalocytes.

Background/aim Tumour necrosis factor-alpha (TNF alpha) 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 TNF alpha on the functional properties of hyalocytes is unknown. Methods Hyalocytes were isolated from bovine eyes. Cellular proliferation, migration and gel contraction in response to TNF alpha 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 TNF alpha promoted proliferation, migration and gel contraction by hyalocytes. Dexamethasone inhibited TNF alpha-induced proliferation but not migration. Dexamethasone did not inhibit TNF alpha-induced gel contraction but further increased contraction. Furthermore, dexamethasone inhibited TNF alpha-induced extracellular signal-related kinase (ERK) 1/2 phosphorylation in hyalocytes. Conclusion This study indicates that TNF alpha 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.