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Br J Ophthalmol 2009;93:1020-1026 doi:10.1136/bjo.2008.155069
  • Original Article
  • Clinical science

Possible contribution of hyalocytes to idiopathic epiretinal membrane formation and its contraction

  1. R-i Kohno1,
  2. Y Hata1,
  3. S Kawahara1,
  4. T Kita1,
  5. R Arita1,
  6. Y Mochizuki1,
  7. L P Aiello2,3,
  8. T Ishibashi1
  1. 1
    Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  2. 2
    Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA
  3. 3
    Research Division and Beetham Eye Institute, Joslin Diabetes Center, Boston, Massachusetts, USA
  1. Correspondence to Dr Y Hata, Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; hatachan{at}med.kyushu-u.ac.jp
  • Accepted 13 February 2009
  • Published Online First 7 May 2009

Abstract

Aim: To address the cellular components and the contractile mechanisms of the idiopathic epiretinal membrane (ERM).

Methods: Ten surgically removed ERMs were fixed in 4% paraformaldehyde and analysed by whole-mount immunohistochemistry with anti-glial fibrillar acidic protein (GFAP) and alpha smooth-muscle actin (αSMA) antibodies. Type I collagen gel contraction assay, an established wound-healing assay in vitro, was performed using cultured bovine hyalocytes or normal human astrocytes (NHA) to evaluate the contractile property of the cells in the presence of tissue growth factor (TGF)-β2. The expression of αSMA was also analysed by western blot analysis to examine myofibroblastic transdifferentiation of the cells. Vitreous-induced collagen gel contraction was also evaluated.

Results: All membranes were composed of αSMA immunopositive cells in contracted foci and GFAP immunopositive cells in the periphery. No apparent double positive cells were observed in any membranes examined. Cultured hyalocytes showed overexpression of αSMA and hypercontraction of collagen gels in response to TGF-β2, while glial cells showed marginal change. The vitreous from ERM patients also caused overexpression of αSMA and hypercontraction of the gels embedding hyalocytes, which were almost completely inhibited in the presence of anti-TGF-β2 neutralising antibody.

Conclusions: Hyalocytes might be one of the critical components of ERM mediating its contractile property through the effect of TGF-β2 in the vitreous fluid.

Footnotes

  • Funding This study was supported in part by grants from the Ministry of Education, Science, Sports and Culture, Japan (Grant-in-Aid for Scientific Research #19592026).

  • Competing interests None.

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

  • Patient consent Obtained.

  • See Editorial, p 989

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