Abstract
Diabetic retinopathy (DR) is a severe diabetes-induced eye disease, in which its pathological phenomena basically include abnormal proliferation, migration, and angiogenesis of microvascular endothelial cells in the retina. Long non-coding RNAs (lncRNAs) have been proven to be important regulators in various biological processes, but their participation in DR remains largely undiscovered. In the present study, we aimed to unveil the role of lncRNA small nucleolar RNA host gene 16 (SNHG16) in regulating the functions of human retinal microvascular endothelial cells (hRMECs) under a high-glucose (HG) condition. We found that SNHG16 expression was significantly upregulated in hRMECs treated with HG. Functionally, SNHG16 could facilitate hRMEC proliferation, migration, and angiogenesis. Moreover, SNHG16 was associated with nuclear factor κB (NF-κB) and phosphatidylinositol 3-kinase (PI3K)/AKT pathways. Mechanistically, SNHG16 could promote hRMEC dysfunction by sequestering microRNA (miR)-146a-5p and miR-7-5p to act as a competing endogenous RNA (ceRNA) with interleukin-1 receptor-associated kinase 1 (IRAK1) and insulin receptor substrate 1 (IRS1). In conclusion, our results illustrated the potential role of SNHG16 in facilitating hRMEC dysfunction under HG treatment, providing a novel approach for DR therapy.
Highlights
Diabetic retinopathy (DR) is a typical microvascular complication of diabetes mellitus
small nucleolar RNA host gene 16 (SNHG16) expression is upregulated in human retinal microvascular endothelial cells (hRMECs) under HG condition At first, we evaluated cell viability and proliferation under HG condition for 12 h and 48 h
The morphology of hRMECs treated with low glucose (LG) or HG was observed under a microscope
Summary
Diabetic retinopathy (DR) is a typical microvascular complication of diabetes mellitus. Dysfunction of retinal endothelial cells plays an important role in the progression of many vasculopathies, including DR.[5] the prevalence of DR is closely associated with diabetes duration, hypertension, and hyperglycemia. These risk factors can lead to pathological endothelial cell dysfunction, such as excessive proliferation, migration, and angiogenesis of endothelial cells. These abnormal behaviors can subsequently result in pathological retinal neovascularization during the proliferative stage of DR, which can gradually develop into blurred vision, severe visual impairment, and eventually result in blindness.[6,7,8] our research was aimed at exploring the mechanism in regulating the behaviors of human retinal microvascular endothelial cells (hRMECs) cultured under high-glucose (HG) stimulation, imitating DR circumstances
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