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Role of tumour necrosis factor-α (TNFα) in the functional properties of hyalocytes
  1. Yasuaki Hata1,
  2. Shintaro Nakao1,
  3. Ri-ichiro Kohno1,
  4. Kumiyo Oba1,
  5. Takeshi Kita1,
  6. Muneki Miura1,
  7. Yukio Sassa1,
  8. Alexander Schering2,
  9. Tatsuro Ishibashi1
  1. 1Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Higashi-Ku, Fukuoka, Japan
  2. 2Angiogenesis Laboratory, Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA
  1. Correspondence to Dr Tatsuro Ishibashi, Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka 812-8582, Japan; ishi{at}


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.

  • Vitreoretinal diseases
  • inflammation
  • hyalocytes
  • steroid
  • vitreous
  • retina
  • inflammation
  • experimental and laboratory

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  • Funding The study was supported in part by grants from the Ministry of Education, Science, Sports and Culture, Japan (Grant-in-Aid for Scientific Research #21592233).

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval Ethics approval was provided by the Kyushu University Hospital Review Board.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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