The Effects of Ozurdex® (Dexamethasone Intravitreal Implant) on Experimental Proliferative Vitreoretinopathy

2015 ◽  
Vol 233 (3-4) ◽  
pp. 198-203 ◽  
Author(s):  
Hsi-Kung Kuo ◽  
Yi-Hao Chen ◽  
Pei-Chang Wu ◽  
Yu-Hsia Kuo

Purpose: To investigate a new sustained-release formulation of dexamethasone (Ozurdex®) for inhibiting proliferative vitreoretinopathy (PVR) and its effect on the expression of retinal glial reaction and inflammation in experimental PVR eyes. Methods: We used 30 pigmented rabbits for this study. One week after gas compression, the eyes were injected with 5 × 104 retinal pigment epithelial cells into the vitreous cavity to induce PVR. Concurrently, one eye also received an intravitreal injection of Ozurdex; the other eye was used as a control. PVR was graded by indirect ophthalmoscopy on days 1, 3, 7, 14, 21, and 28. The expression of the retinal glial reaction and inflammation in experimental PVR eyes were evaluated by Western blot analysis. Results: PVR severity increased gradually and peaked after 14 days, and no differences in PVR severity between the study and control groups were observed at any time point. The expression of glial fibrillary acid protein (GFAP) increased on days 7 and 14 in both the PVR control and study groups. While the use of Ozurdex in the study group showed less GFAP expression, this difference was not significant. The expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 significantly increased on days 7 and 14 in PVR control eyes. There was a significant difference in TNF-α between PVR control eyes and Ozurdex-treated eyes on days 7 (p < 0.001) and 14 (p = 0.019). Ozurdex in the study group showed lower IL-6 expression; however, this difference was not significant on days 7 (p = 0.063) and 14 (p = 0.052). Conclusions: The intravitreal injection of Ozurdex suppressed the expression of inflammatory markers; however, it did not mitigate the severity of experimental PVR in this animal model.

2019 ◽  
Vol 71 (1) ◽  
pp. 175-182 ◽  
Author(s):  
Wojciech Garczorz ◽  
Enrique Gallego-Colon ◽  
Agnieszka Kosowska ◽  
Krzysztof Siemianowicz ◽  
Agnieszka Kłych-Ratuszny ◽  
...  

2015 ◽  
Vol 99 (5) ◽  
pp. 700-704 ◽  
Author(s):  
Nicoline M Korthagen ◽  
Kiki van Bilsen ◽  
Sigrid M A Swagemakers ◽  
Jeroen van de Peppel ◽  
Jeroen Bastiaans ◽  
...  

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10136
Author(s):  
Hui Zou ◽  
Chenli Shan ◽  
Linlin Ma ◽  
Jia Liu ◽  
Ning Yang ◽  
...  

Under physiological conditions, retinal pigment epithelium (RPE) is a cellular monolayer composed of mitotically quiescent cells. Tight junctions and adherens junctions maintain the polarity of RPE cells, and are required for cellular functions. In proliferative vitreoretinopathy (PVR), upon retinal tear, RPE cells lose cell-cell contact, undergo epithelial-mesenchymal transition (EMT), and ultimately transform into myofibroblasts, leading to the formation of fibrocellular membranes on both surfaces of the detached retina and on the posterior hyaloids, which causes tractional retinal detachment. In PVR, RPE cells are crucial contributors, and multiple signaling pathways, including the SMAD-dependent pathway, Rho pathway, MAPK pathways, Jagged/Notch pathway, and the Wnt/β-catenin pathway are activated. These pathways mediate the EMT of RPE cells, which play a key role in the pathogenesis of PVR. This review summarizes the current body of knowledge on the polarized phenotype of RPE, the role of cell-cell contact, and the molecular mechanisms underlying the RPE EMT in PVR, emphasizing key insights into potential approaches to prevent PVR.


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