Role of tumour necrosis factor- (TNF ) in the functional properties of hyalocytes
| Autor: | Kumiyo Oba, Ri Ichiro Kohno, Yasuaki Hata, Tatsuro Ishibashi, Shintaro Nakao, Yukio Sassa, Alexander Schering, Muneki Miura, Takeshi Kita |
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| Rok vydání: | 2010 |
| Předmět: |
MAPK/ERK pathway
medicine.medical_specialty Necrosis medicine.medical_treatment Blotting Western Anti-Inflammatory Agents Dexamethasone Proinflammatory cytokine Pathogenesis Cellular and Molecular Neuroscience Retinal Diseases Internal medicine medicine Animals Cells Cultured Cell Proliferation Cell Size Tumor Necrosis Factor-alpha business.industry Kinase Macrophages Recombinant Proteins Sensory Systems Vitreous Body Ophthalmology Cytokine Endocrinology Cytokines Cattle Tumor necrosis factor alpha medicine.symptom Cell Migration Assays business Signal Transduction medicine.drug |
| Zdroj: | British Journal of Ophthalmology. 95:261-265 |
| ISSN: | 0007-1161 |
| DOI: | 10.1136/bjo.2010.190322 |
| Popis: | Background/aim Tumour necrosis factor-a (TNFa )i s 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 TNFa on the functional properties of hyalocytes is unknown. Methods Hyalocytes were isolated from bovine eyes. Cellular proliferation, migration and gel contraction in response to TNFa 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 TNFa promoted proliferation, migration and gel contraction by hyalocytes. Dexamethasone inhibited TNFa-induced proliferation but not migration. Dexamethasone did not inhibit TNFa-induced gel contraction but further increased contraction. Furthermore, dexamethasone inhibited TNFa-induced extracellular signal-related kinase (ERK)1/2 phosphorylation in hyalocytes. Conclusion This study indicates that TNFa 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. |
| Databáze: | OpenAIRE |
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