Fig 2: The knockdown of SRGN significantly promoted HREC proliferation after high‐glucose treatment. A, Cell proliferation after treated with high glucose and transfection with siRNA1‐SRGN. B, Cell proliferation after treated with high glucose and transfection with siRNA2‐SRGN. Control, untreated HRECs with 5.5 mmol/L glucose

Fig 3: ROC analysis of SRGN for the diagnosis of DR. A, The potential of SRGN for distinguishing DR patients from T2DM patients. AUC = 0.7680, the sensitivity of 47.27%, specificity of 100%, and cutoff value of 1.4727. B, The potential of SRGN for distinguishing DR patients from healthy controls. AUC = 0.8753, the sensitivity of 69.23%, specificity of 100%, and cutoff value of 1.6923. ROC, receiver operating characteristic

Fig 4: Comparison of SRGN levels in HRECs after treated with glucose. A, mRNA expression of SRGN measured by qPCR assay. B, Protein bands of SRGN measured by Western blot assay. C, The quantified result of B was presented. ** p < 0.01, high glucose vs. control group. Control, untreated HRECs with 5.5 mmol/L glucose; high, HRECs treated with 30 mmol/L glucose; HRECs, human retinal endothelial cells

Fig 5: The knockdown of SRGN significantly inhibited HREC apoptosis after high‐glucose treatment. A, The cell apoptosis after treated with high glucose and transfection with siRNA1‐SRGN. B, The cell apoptosis after treated with high glucose and transfection with siRNA2‐SRGN. * p < 0.05, HG + siRNA1(2)‐SRGN vs HG + siRNA‐NC group; ** p < 0.01, HG vs control group; control, untreated HRECs with 5.5 mmol/L glucose