Erratum to "Epac1 Restores Normal Insulin Signaling through a Reduction in Inflammatory Cytokines".

[This corrects the article DOI: 10.1155/2018/3809092.].

Epac1 Restores Normal Insulin Signaling through a Reduction in Inflammatory Cytokines.

We have previously reported that Epac1 reduced inflammatory cytokines, which is protective to the diabetic retina. We have also published that impaired insulin signaling occurs in the diabetic retina. A reduction in interleukin-1 beta (IL-1) and tumor necrosis factor alpha (TNF) by Epac1 could potentially restore normal insulin signal transduction.

miR15a regulates NLRP3 inflammasome proteins in the retinal vasculature.

We have previously published that miR15a can reduce inflammatory cytokines, which could be key to diabetic retinal pathology. In this work, we wanted to investigate whether miR15a altered NLR pyrin domain 3 (NLRP3) proteins. Whole retinal lysates from both miR15a overexpressing mice and endothelial cell specific miR15a/16 knockout mice were used to investigate protein levels of forkhead box protein O1 (Foxo1), NLRP3, cleaved caspase 1 and interleukin-1 beta (IL-1β).

TLR4 regulates insulin-resistant proteins to increase apoptosis in the mouse retina.

Objective And Design: Work in multiple organs has suggested that toll-like receptor 4 (TLR4) may play a role in insulin resistance. Additional studies have shown a negative role for TLR4 on retinal health. We have previously reported that β-adrenergic receptors can regulate both TLR4 signal transduction, as well as insulin signaling in the retina and in retinal endothelial cells.

Epac1 Blocks NLRP3 Inflammasome to Reduce IL-1 in Retinal Endothelial Cells and Mouse Retinal Vasculature.

Inflammation is an important component of diabetic retinal damage. We previously reported that a novel -adrenergic receptor agonist, Compound 49b, reduced Toll-like receptor 4 (TLR4) signaling in retinal endothelial cells (REC) grown in high glucose. Others reported that TLR4 activates high-mobility group box 1 (HMGB1), which has been associated with the NOD-like receptor 3 (NLRP3) inflammasome.