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Wiley, Acta Ophthalmologica, (90), p. 0-0, 2012

DOI: 10.1111/j.1755-3768.2012.s085.x

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Early reactional hyperplasia and neuronal differentiation of the ciliary epithelium (CE) in experimental retinal detachment (RD) with proliferative vitreoretinopathy (PVR) in the porcine eye

This paper is available in a repository.
This paper is available in a repository.

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Data provided by SHERPA/RoMEO

Abstract

Background: Rare quiescent retinal progenitor cells have been isolated in the adult amphibian ciliary marginal zone (Hollyfield, 1968), then in the mammalian (Tropepe et al, 2000) (Ahmad et al, 2000) (Fischer and Rey, 2000) and human CE (Coles et al, 2004) (Ballios et al, 2011). This contingent might be inhibited in the adult eye by the signaling pathway ephrin (Chen, personal communication, ARVO 2012, submitted, Stem Cells). Retinal injury might be a triggering factor to quit the dormant state in the adult mammalian CE (Ooto, 2004) (Nickerson, 2007) (Nishiguchi 2008) (Kiyama et Wang, 2010), as it has been demonstrated also in the human brain (Moe et al, 2005) (Logan et al, 2006) . We have reported a CE proliferation with retinal neuronal and photoreceptor differentiation in three human eyes eviscerated for longstanding RD and PVR (Ducournau et al 2012). The CE strongly expressed EGFR. The concept of niche (Fischer and Rey, 2003) is now well established in stem cells recruitment processes. We have hypothezised that the disease RD and PVR might stimulate a dormant population of Retinal Progenitor Cells (RPCs) in the CE in the human eye in vivo in presence of a niche constituted by EGF. Proliferation in the ciliary body, together with nestin expression in ciliary MCM2+ (macrophage/microglia marker F4/80) cells were found in mice eyes with experimental RD, suggesting that RD might activate putative RPCs (Suburo et al, 2010). The aim of the present work was to study the CE in the porcine eye with experimental DR and PVR.