Surgical treatment for neovascularized retinal pigment epithelial detachment in age -related macular degeneration

Dear Sir, I am Dr. Hui Li, from the Department of Ophthalmology of Shanghai Tenth People’s Hospital Affiliated to Tongji University in Shanghai, China. I write to report a case of neovascularized pigment epithelial detachment (PED) successfully treated with vitrectomy. PED associated occult choroidal neovascular membrane, so called vascularized PED [1] , is a special subtype of neovascular age-related macular degeneration with poor

Down-regulation of protein kinase C alpha/ezrin signals in light-induced phagocytic crisis of retinal pigment epithelium cells

AIM： To investigate the roles of PKC-α/ezrin signals in phagocytosis crisis of retinal pigment epithelium（RPE） cells in light damage model. METHODS： Light induced mice RPE injury model was established by continuously irradiating cool white light at different exposure time（0, 4, 8h light intensity： 4.18×10^-6 J/cm^2）. In vitro, human ARPE-19 cells treated with the doses and intensity（1.57×10^-6 J/cm^2） of laser irradiation. Histology analysis was evaluated by hematoxylin and eosin（HE） staining. In vivo RPE phagocytosis was quantified by measuring the accumulation of photoreceptor outer segments in the sub-retinal space. In vitro RPE phagocytosis was assessed by calculating the relative fluorescence intensity of FITC-labeled microspheres in ARPE-19 cells. To further investigate the molecular mechanism, the activation of PKC-α/ezrin signal was evaluated by Western blot in vivo and in vitro.RESULTS： HE staining revealed that the thickness of outer nuclear layer decreased significantly after 4 and 8h light exposure. By immunostaining with rhodopsin, a significant greater accumulation of photoreceptor outer segment was noticed after light injury. In vitro, light injuredRPE cells had less phagocytic activity in a dose dependent manner than that of the normal control（P〈0.01）. Western blot suggested the activation of PKC-α/ezrin signaling was down-regulated in a dose-dependent manner after light exposure. CONCLUSION： Our data suggest that light induced phagocytic crisis of RPE cells may result from the downregulation of PKC-α/ezrin signaling.

Endoplasmic reticulum-mitochondrial crosstalk:a novel role for the mitochondrial peptide humanin

In this review,the interactive mechanisms of mitochondria with the endoplasmic reticulum（ER） are discussed with emphasis on the potential protective role of the mitochondria derived peptide humanin（HN） in ER stress.The ER and mitochondria are dynamic organelles capable of modifying their structure and function in response to changing environmental conditions.The ER and mitochondria join together at multiple sites and form mitochondria-ER associated membranes that participate in signal transduction pathways that are under active investigation.Our laboratory previously showed that HN protects cells from oxidative stress induced cell death and more recently,described the beneficial role of HN on ER stress-induced apoptosis in retinal pigment epithelium cells and the involvement of ER-mitochondrial cross-talk in cellular protection.The protection was achieved,in part,by the restoration of mitochondrial glutathione that was depleted by ER stress.Thus,HN may be a promising candidate for therapy for diseases that involve both oxidative and ER stress.Developing novel approaches for retinal delivery of HN,its analogues as well as small molecular weight ER stress inhibitors would prove to be a valuable approach in the treatment of age-related macular degeneration.