Copyright: ©Author(s) 2026.
World J Diabetes. Mar 15, 2026; 17(3): 115433
Published online Mar 15, 2026. doi: 10.4239/wjd.v17.i3.115433
Published online Mar 15, 2026. doi: 10.4239/wjd.v17.i3.115433
Figure 6 PRDX2 silencing inhibits RhoA/ROCK signaling in Müller cells.
A: Tandem mass tagging proteomics of PRDX family proteins, RhoA, RhoGDI1, nestin in shPRDX2 and shNC groups; B and C: Protein expression of PRDX2, RhoA, ROCK1/2, and RhoGDI1 between shPRDX2 and shNC groups after high glucose- or normal glucose-treated rMC-1 cells for 48 hours by western blotting; D-F: The bar histograms represent measurements of the target protein's gray values. All values are presented as means ± SEM. Each experiment was independently repeated three times. P for trends assessed using the t test or ordinary one-way analysis of variance. aP < 0.05; bP < 0.01; cP < 0.001; dP < 0.0001. TMT: Tandem mass tag; NG: Normal glucose; HG: High glucose.
- Citation: Du XL, Ouyang S, Wang YS, Mao YS, Ren BC, Yu WH. PRDX2 silencing alleviates reactive hyperplasia of Müller glial cells in diabetic retinopathy by inhibiting the RhoA/ROCK signaling pathway. World J Diabetes 2026; 17(3): 115433
- URL: https://www.wjgnet.com/1948-9358/full/v17/i3/115433.htm
- DOI: https://dx.doi.org/10.4239/wjd.v17.i3.115433