Expression of microRNA‑155‑5p in patients with refractory diabetic macular edema and its regulatory mechanism

Abstract

Diabetic macular edema (DME) is the main cause of visual impairment in diabetic patients, but its pathogenesis remains unclear. The purpose of the present study was to analyze the expression of microRNA (miR)-155-5p in patients with DME and its regulatory mechanism. A total of 72 patients diagnosed with DME and 17 with idiopathic macular hole (MH) were recruited. Among samples from patients with DME, 45 were DME and 27 were refractory DME, whereas patients with idiopathic MH served as the control group. Optical coherence tomography and fundus photograph analysis revealed that part of the retina in the fundus of patients with DME was thickened, with macular edema occurring simultaneously. In refractory patients with DME, macular edema was associated with bleeding and a dark cavity between retinal layers. Through reverse transcription-quantitative PCR analysis, miR-155-5p was highly expressed in the aqueous humor (AH) and plasma of patients with DME compared with that in patients with MH, and this was even higher in the refractory DME group. Upon analyzing patient clinical data, the difference in miR-155-5p expression in the AH and plasma was positively associated with disease course, body mass index, fasting blood-glucose, glycated hemoglobin, proteinuria and glycosuria. The expression of miR-155-5p was not significantly different based on hemoglobin, intraocular pressure and sex. The aforementioned results indicate that miR-155-5p might promote the development of DME. To further study the molecular mechanism, human retinal microvascular endothelial cells (HRMECs) were cultured and treated with high glucose in vitro. The results showed that miR-155-5p expression was significantly upregulated in HRMECs induced by high glucose. After inhibiting the expression of miR-155-5p, cell proliferation, angiogenesis and VEGF protein levels were significantly downregulated, whereas miR-155-5p mimics had the opposite effect. In summary, miR-155-5p is closely associated with DME and is a potential target for refractory DME treatment.

Identifying miRNA Signatures Associated with Pancreatic Islet Dysfunction in a FOXA2-Deficient iPSC Model

“…Also, some of the DEmiRs are associated with diabetes complications, such as miR-133a-3p, which is associated with myocardial steatosis in T2D patients [76], and miR-129-2-3p [77] and miR-129-5p, which have been detected in T2D patients with macrovascular complications [78]. Furthermore, hsa-miR-155-5p is closely associated with diabetic macular edema (DME) [79]. Several upregulated miRNAs are detected to be associated with diabetic nephropathy (DN) patients such as, miR-372-3p [47], miR-548ah-3p, miR-760 [80], and miR-1269b [81].…”

Mini‐αA Upregulates the miR‐155‐5p Target Gene CDK2 and Plays an Antiapoptotic Role in Retinal Pigment Epithelial Cells during Oxidative Stress

“…During corneal wound healing, miR-155-5p reduces corneal epithelial permeability by reshaping tight epithelial junctions [ 38 ]. In diabetic macular edema, the inhibition of miR-155-5p expression downregulates cell proliferation, angiogenesis, and vascular endothelial growth factor levels [ 39 ]. These studies demonstrate that miR-155-5p can potentially be used as a biomarker for eye-related diseases.…”

Effect of Shuangdan Mingmu Capsule on Diabetic Retinopathy in Rats via Regulation of miRNAs

“…Numerous studies have shown that miR-155-5p plays an important role in the progression of diabetes. 50 , 51 It regulates the proliferation and angiogenesis of HRMECs (human retinal endothelial cells) and simultaneously affects the protein level of VEGF-A in HRMECs. Our previous findings indicated that SDMM capsules inhibit angiogenesis by suppressing the expression of the VEGF family, including VEGF-A.…”