Abstract
Purpose :
Cytokine-mediated pericyte loss is a cornerstone in the development of diabetic macular edema (DME) among non-proliferative diabetic retinopathy (NPDR). In vitro, TGF-β increased expression leads to pericytal apoptosis and macular edema (through the breakdown in the blood-retinal barrier). To date, there are no reports on TGF-b expression in vivo. Here, we assessed the relationship between TGF-β1 and -β2 expression levels in plasma and aqueous humor (AH) of patients with NPDR with and without DME.
Methods :
We performed a case-control study of 53 patients clinically diagnosed with NPDR. Cases had a recent diagnosis of DME and were starting an antiangiogenic treatment. Controls were patients without EMD undergoing phacoemulsification for senile cataracts. We measured visual acuity, LOCS-III and RDNP staging, macular OCT, HbA1c, and collected serum and aqueous humor samples. We measured the concentration of TGF-β1 and -β2 by cytometric-bead assays. We performed a Student's T-test and linear regressions to adjust our results with SAS V 9.4.
Results :
DME cases have significantly more TGF-β1 and -β2 AH expression compared to non-DME (Mean difference pg/µL: 440.5 and 110.1, respectively, p < 0.001). Moreover, there was a positive correlation between TGF-β and macular thickness, especially among those with spongiform changes. There was no significant correlation between the levels of TGF-β in AH and serum, which suggests that the effect generated by these cytokines could be a local process.
Conclusions :
Our findings suggest that aqueous humor TGF-β1 expression levels are associated with macular edema in patients with nonproliferative diabetic retinopathy. The predictive capacity of TGF-β1 warrants further study.
This is a 2020 ARVO Annual Meeting abstract.