Differences in genotype distributions between patients with RRD with or without PVR were detected in rs1800795 (IL6) (P = 0.04), rs1800871 (in the vicinity of the IL10) (P = 0.034), and rs1800471 (TGFB1) (P = 0.032).
<i>Purpose</i>: Comparison of IL-6 and CXCL-1 concentrations and CXCL-1/IL-6 ratio correlations with clinical parameters (RRD extent, duration, and proliferative vitreoretinopathy - PVR-grade) between subretinal fluid (SRF) and vitreous during rhegmatogenous retinal detachment (RRD) complicated with PVR.<i>Methods</i>: A total of 71 eyes of 71 patients with primary RRD possibly complicated with PVR were included; 36 eyes treated with scleral buckling and 35 eyes with pars-plana vitrectomy.
Differences in genotype distributions between patients with RRD with or without PVR were detected in rs1800795 (IL6) (P = 0.04), rs1800871 (in the vicinity of the IL10) (P = 0.034), and rs1800471 (TGFB1) (P = 0.032).
BK had effects in TGF‑β1‑induced EMT by upregulating the expression of Smad7 and downregulating the expression of pSmad3 in TGF‑β/Smad signaling pathway, indicating that BK may be a novel and effective therapy for PVR.
PTN is involved in the process of EMT induced by TGF-β1 in human ARPE-19 cells in vitro, and PTN knockdown attenuated the progression of experimental PVR in vivo.
PVR is associated with a cytokine storm involving common proinflammatory molecules like IL6, but little is known about the source and downstream signaling of IL6 and the consequences for the retina.
To examine the effect of Notch inhibition on TGF-β1-induced EMT and PVR formation, ARPE-19 cells were preincubated with γ-secretase inhibitor LY411575 before TGF-β1 treatment.
EGCG and curcumin are potent in preventing EMT induced by TGF-β1 in ARPE-19 cells and therefore, proposed as potential molecules for further pre-clinical evaluation in PVR management.
This study describes the regulation of EMT in RPE cells by TGF-β1/miR-124/RHOG signaling and suggests that the supplement of miR-124 exogenously would be a valuable therapeutic approach for the prevention or treatment of proliferative vitreoretinopathy.
Proliferative vitreoretinopathy vitreous stimulated the production of chemokine (C-C motif) ligand (CCL)2, chemokine (C-X-C motif) ligand (CXCL)8, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-6, and platelet-derived growth factor (PDGF)-BB by ARPE-19 to significantly (P < 0.05) higher levels than vitreous from the RRD1 and RRD2 groups.
Interleukin-6 and genes that were related to melanogenesis were expressed in the proliferative membranes and may play an important role in the generation of proliferative vitreoretinopathy.
The presence of IL-1 beta, IL-6 and TNF alpha mRNA-positive cells within retinal membranes provides further evidence of a pathogenic role of these cytokines in proliferative vitreoretinopathy.
In conclusion, the CRISPR/dCas9 capability for blocking TGF-β2-induced expression of MDM2 and EMT biomarkers can be exploited for a therapeutic approach to PVR.