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Shoji Notomi, Toshio Hisatomi, Yusuke Murakami, Atsunobu Takeda, Yasuhiro Ikeda, Hiroshi Enaida, Tatsuro Ishibashi; Extracellular ATP accelerates photoreceptor cell death via ligation of P2X7 receptor in retinal detachment. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4195.
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Extracellular ATP is released from damaged tissue and acts on P2X purinergic receptor. Recently, ATP has been known as a damage-associated molecular pattern (DAMP) molecule which can participate neurodegenerative processes via induction of specific inflammatory responses. We investigated the role of extracellular ATP as a DAMP molecule in an animal model of retinal detachment.
We compared ATP levels of vitreous samples from patients with rhegmatogenous retinal detachment (RRD) to those of macular hole (MH) or epi-retinal membrane (ERM). The ATP concentrations were quantified by luciferase assay. We tested whether extracellular ATP is involved in neuroinflammation by means of primary retinal cell cultures and a rodent model of retinal detachment. We also examined the effect of pharmacological blockade or genetic deficiency of P2X7 on photoreceptor death caused by retinal detachment.
The ATP levels in vitreous samples of patients with RRD were significantly higher than those of MH or ERM. Extracellular ATP induced a significant decline of photoreceptor viability in primary retinal cell cultures. Inflammatory cytokines as well as TUNEL-detectable photoreceptor apoptosis was significantly reduced by pharmacological blockade or genetic deficiency of P2X7 in retinal detachment.
Extracellular ATP accelerates inflammatory responses and photoreceptor apoptosis in retinal detachment. Pharmacological P2X7 blockade may provide potential therapeutic effects in retinal detachment.
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