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      Ocular pathogenesis and immune reaction after intravitreal dispase injection in mice

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      , , ,
      Molecular Vision
      Molecular Vision

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          Abstract

          Purpose

          The purpose of the current study was to examine the ocular pathogenesis and immune reaction in mice after intravitreal dispase injection.

          Methods

          Three microliters of dispase at a concentration of 0.2 U/μl were injected into the vitreal cavities of 4–6-week-old mice. Hematoxylin and eosin staining, immunofluorescence analysis, and electroretinograms of the eyes were then performed to assess ocular changes, and enzyme-linked immunospot assays and intracellular staining of single-cell suspensions of the spleens were used to detect immune changes during an 8 week observation period.

          Results

          Neutrophils were the main inflammatory infiltrating cells appearing at the anterior chamber. No cluster of differentiation (CD)3+ labeled T cells, F4/80+ labeled macrophages, or CD56+ labeled natural killer cells were found in the vitreal cavities or retinas in dispase-injected mice within 5 days after injection. Proliferative vitreoretinopathy (PVR)-like signs first appeared at 2 weeks, gradually increased thereafter, and reached peak values at 8 weeks. There was a statistically significant difference in b-wave amplitudes between the PVR and saline-control eyes. Enzyme-linked immunospot assays and intracellular staining showed that specific CD4+ and CD8+ labeled T cells were not involved in dispase-injected mice.

          Conclusions

          Our data show that neutrophils in the anterior chamber and PVR-like signs in the retinas were found, and that specific immune reactions were not involved after intravitreal dispase injection in mice.

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          Most cited references43

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          Proliferative vitreoretinopathy: risk factors and pathobiology.

          Proliferative vitreoretinopathy (PVR) is still a major cause of failure of retinal detachment surgery. Despite a dramatic increase in our pathobiologic knowledge of PVR during the last 10 years, little of this information has been used to modify the surgical management of the disease, and, thus, the anatomic and functional results are still unsatisfactory. Collaborative research involving clinicians and basic researchers must be encouraged. PVR must be considered a multifactorial disease caused by interaction of several cells and intra- and extraocular factors. Therefore, therapeutic options based on the inhibition of one factor or phenomenon may be regarded with scepticism. To prevent PVR, it is necessary to determine the factors involved in its development, and because of its relatively small prevalence, large, prospective, multicenter studies seem necessary. In addition, clinical research must not be underestimated. PVR affects both sides of the retina and the retina itself, a point to which little attention has been paid and that is critical for surgical results. Therefore, a new classification that provides information about clinical relevance, such as the evolutionary stages of the disease (biologic activity) and the degree of surgical difficulty (location of the fibrotic process), seems necessary.
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            Standard for clinical electroretinography (2004 update).

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              Proliferative vitreoretinopathy: an overview.

              Proliferative vitreoretinopathy (PVR) is still the most common cause of failure of surgery for rhegmatogenous retinal detachment, despite the substantial effort that has been devoted to better understanding and managing this condition during the past 25 years. Basic research has indicated that PVR represents scarring, the end stage of the wound-healing process that occurs after retinal detachment surgery. Medical treatment has been directed toward preventing inflammation, the first phase of the wound healing process, and inhibiting cell proliferation, the second phase. The 1983 Retina Society classification was modified in 1989 by the Silicone Study Group, whose classification differentiates between posterior and anterior forms of PVR and recognizes three patterns of proliferation: diffuse, focal, and subretinal. The anterior form has a worse prognosis than the posterior form, and its treatment requires more complex surgical procedures. In this review, risk factors and pathobiology of PVR are discussed, and management of PVR of various degrees of severity are considered.
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                Author and article information

                Journal
                Mol Vis
                Mol. Vis
                MV
                Molecular Vision
                Molecular Vision
                1090-0535
                2012
                07 April 2012
                : 18
                : 887-900
                Affiliations
                [1]State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
                Author notes

                The first two authors contributed equally to this work

                Correspondence to: Qianying Gao, State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, 510060, China; Phone: (0086)-(020)-87330490; FAX: (0086)-(020)-87333271; email: gaoqy@ 123456mail.sysu.edu.cn
                Article
                93 2011MOLVIS0279
                3327440
                22511850
                c3a4ab3c-bf0a-4eb2-bacc-e1634a6b9774
                Copyright © 2012 Molecular Vision.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 June 2011
                : 04 April 2012
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                Vision sciences
                Vision sciences

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