RT Journal Article
SR Electronic
T1 Role of tumour necrosis factor-α (TNFα) in the functional properties of hyalocytes
JF British Journal of Ophthalmology
JO Br J Ophthalmol
FD BMJ Publishing Group Ltd.
SP 261
OP 265
DO 10.1136/bjo.2010.190322
VO 95
IS 2
A1 Yasuaki Hata
A1 Shintaro Nakao
A1 Ri-ichiro Kohno
A1 Kumiyo Oba
A1 Takeshi Kita
A1 Muneki Miura
A1 Yukio Sassa
A1 Alexander Schering
A1 Tatsuro Ishibashi
YR 2011
UL http://bjo.bmj.com/content/95/2/261.abstract
AB 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.