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Jingfa Zhang, Tianqin Wang, Chaoyang Zhang, Hai xie, Qiuxue Yi, Dandan Liu, Qing Peng, Weiye Li, Guo-Tong Xu, Lin Liu; Ranibizumab prevents Müller cell edema in diabetic retinopathy. Invest. Ophthalmol. Vis. Sci. 2019;60(9):2653.
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© ARVO (1962-2015); The Authors (2016-present)
To explore the mechanism(s) of ranibizumab targeting Müller glia for intracellular edema in diabetic retinopathy.
Sprague-Dawley rats were rendered diabetes with intraperitoneal injection of streptozotocin. Intravitreal injection of ranibizumab (20 mg/eye) was performed 8 weeks after diabetes onset. Four weeks later, the rats were sacrificed and the retinas were harvested for detection. rMC-1 cells were treated with glyoxal (1 mM) for 24 hours, with or without ranibizumab. Cell viability was detected with CCK-8 assay. The expressions of Kir4.1, Dp71, VEGF-A and Glutamine synthetase were examined with WB. VEGF-A in the supernatant was detected with ELISA. The intracellular potassium and sodium level was detected with the specific probe.
Compared to the normal control, the protein expressions of Kir4.1 and Dp71 were down-regulated significantly in diabetic rat retina, which could be reversed by ranibizumab. The above changes were confirmed with in vitro study. The intracellular potassium level is increased in glyoxal-treated rMC-1 cells compared with that in normal control, while intracellular sodium level, but not potassium, was decreased by ranibizumab.
Ranibizumab, through binding VEGF-A, could maintain the expressions of Kir4.1 and Dp71 to decrease the intracellular osmotic pressure, thus protect Müller cells from swelling.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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