Background Proliferative vitreoretinopathy (PVR) is a blind-causing disease initiated by the activation of retinal pigmented epithelium (RPE) primarily induced by TGF-β families. Migrasome is a recently discovered type of extracellular vesicle related to cell migration. Results Here, we used ex vivo, in vitro, and in vivo models, to investigate the characteristics and functions of migrasomes in RPE activation and PVR development. Results indicated that the migrasome marker tetraspanin-4 (TSPAN4) was abundantly expressed in human PVR-associated clinical samples. The ex vivo model PVR microenvironment is simulated by incubating brown Norway rat RPE eyecups with TGF-β1. Electron microscope images showed the formation of migrasome-like vesicles during the activation of RPE. Further studies indicated TGF-β1 increased the expression of TSPAN4 which results in migrasome production. Migrasomes can be internalized by RPE and increase the migration and proliferation ability of RPE. Moreover, TSPAN4-inhibited RPE cells are with reduced ability of initiating experimental PVR. Mechanically, TSPAN4 expression and migrasome production are induced through TGF-β1/Smad2/3 signaling pathway. Conclusion In conclusion, migrasomes can be produced by RPE under PVR microenvironment. Migrasomes play a pivotal role in RPE activation and PVR progression. Thus, targeting TSPAN4 or blocking migrasome formation might be a new therapeutic method against PVR.

Objectives. To report the long-term results of scleral buckling using 25-gauge chandelier illumination. Methods. The medical records of all patients presenting to Shanghai Tenth People’s Hospital with simple rhegmatogenous retinal detachment (RRD) from June 2013 to Oct 2015 were retrospectively reviewed in this consecutive case series. All patients underwent preoperative and postoperative best corrected visual acuity (BCVA), B-ultrasound, fundus photography, and optical coherence tomography examination. Ultrasound biomicroscopy (UBM) was obtained postoperatively. Results. Ten patients (10 eyes) were included in the final analysis. Of 10 patients, the average age was 49.3 ± 18.9 years old, the average duration of RRD was 30.9 ± 53.3 days, and the mean follow-up period was 6.2 ± 0.9 years. There were nine eyes with myopia and four eyes with macular detachment. The primary anatomical success rate was 90%. Five eyes underwent 360-degree band with element surgery, and five eyes underwent element surgery alone. The average length of encircling band and element was 68.2 ± 1.3  mm and 10.5 ± 2.5  mm, respectively. There were no intraoperative or postoperative complications that occurred. The final BCVA was greater than or equal to 20/40 in nine eyes, of which four eyes achieved 20/20. UBM examination of the 25-gauge chandelier insertion site revealed no tissue proliferation. Conclusions. For simple rhegmatogenous retinal detachment treatment, 25-gauge chandelier illumination-assisted scleral buckling is a kind of effective and safe method.

Background：Proliferative vitreoretinopathy (PVR) is a blind-causing disease initiated by the activation of retinal pigmented epithelium (RPE) primarily induced by TGF-β families. Migrasomes is a recently discovered type of extracellular vesicles related to cell migration. Results: Here, we used ex vivo, in vitro, and in vivo models, to investigate the characteristics and functions of migrasomes in RPE activation and PVR development. Results indicated that the migrasome marker tetraspanin-4 (TSPAN4) was abundantly expressed in human PVR-associated clinical samples. The ex vivo model PVR microenvironment is simulated by incubating brown Norway rat RPE eyecups with TGF-β1. Electron microscope images showed the formation of migrasome-like vesicles during the activation of RPE. Further studies indicated TGF-β1 increased the expression of TSPAN4 which results to migrasome production. Migrasomes can be internalized by RPE and increase the migration and proliferation ability of RPE. Moreover, TSPAN4-inhibited RPE cells are with reduced ability of initiating experimental PVR. Mechanically, TSPAN4 expression and migrasome production is induced through TGF-β1/Smad2/3 signaling pathway. Conclusions：In conclusion, migrasomes can be produced by RPE under PVR microenviroment. Migrasomes play a pivotal role in RPE activation and PVR progression. Thus, targeting TSPAN4 or blocking migrasome formation might be a new therapeutic method against PVR.