Long non-coding RNA SNHG16 contributes to progression of carotid atherosclerosis by regulating miR-30c-5p/ADAM10 axis

Abstract

IntroductionCarotid atherosclerosis (CAS) is one of the main causes of cerebral infarction in the ageing population. Long non-coding RNA small nucleolar RNA host gene 16 (lnc-SNHG16) could promote the development of atherosclerosis. However, the mechanism of lnc-SNHG16 in CAS remains vague.Material and methodsThe expression levels of lnc-SNHG16, microRNA-30c-5p (miR-30c-5p) and disintegrin and metalloproteinase 10 (ADAM10) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays, severally. The levels of interleukin-6 (IL-6), IL-β and tumor necrosis factor-α (TNF-α) were assessed by enzyme-linked immunosorbent assay (ELISA). Protein levels of spinal muscular atrophy (SMA), calponin and ADAM10 were examined by western blot assay. The binding relationship between miR-30c-5p and lnc-SNHG16 or ADAM10 was predicted by Starbase, then verified by the dual-luciferase reporter assay.ResultsLnc-SNHG16 and ADAM10 were increased, and miR-30c-5p was decreased in CAS patient and oxidized low-density lipoprotein (ox-LDL)-treated human aortic smooth muscle cells (hASMCs). Lnc-SNHG16 silencing repressed cell viability, migration, inflammation, facilitated differentiation in ox-LDL-treated hASMCs. Moreover, mechanical analysis proved that lnc-SNHG16 improved ADAM10 expression by sponging miR-30c-5p.ConclusionsOur data indicated that lnc-SNHG16 could regulate the progression of ox-LDL induced CAS model by the miR-30c-5p/ADAM10 axis, implying a potential therapeutic strategy for CAS

Role of Lnc-RNAs in the Pathogenesis and Development of Diabetic Retinopathy

“…This suggests that the cPWWP2A-miR-579angiopoietin 1/occludin/SIRT1 network regulates retinal vascular dysfunction in vivo (Figure 2) [84]. contribute to DR by sponging miR-939 to target VEGF expression, thus regulating activation of the PI3K/AKT pathway in RPE cells [72]. SIRT1: After HG treatment of RPE cells, MEG3 promotes the expression of Sirt1 by acting as a sponge for miR-34a, thus inhibiting the activation of the NF-κB pathway triggered by HG and inhibiting the activation of Müller cells as well as the inflammatory response and apoptosis [41].…”

“…MicroRNA miR-939 might be a downstream target of HEIH, and VEGF was identified as a target of miR-939. VEGF activation triggers the PI3K/AKT signaling pathway, leading to the development and progression of DR. Research showed that the suppression of HEIH inhibited HG-induced activation of the PI3K/AKT signaling pathway, suggesting that HEIH may contribute to DR by sponging miR-939 to target VEGF expression and by regulating activation of the PI3K/AKT pathway [ 72 ].…”

Crosstalk between MiRNAs/lncRNAs and PI3K/AKT signaling pathway in diabetes mellitus: Mechanistic and therapeutic perspectives

“…Overall, their investigation unveiled a potential implication of HEIH in the progression of DR, achieved through its role as a miR-939 sponge targeting VEGF expression, as well as its influence on the modulation of PI3K/AKT pathway activation. Collectively, the HEIH/miR-939/VEGF axis may offer a fresh and innovative avenue for the exploration of therapeutic strategies in the context of DR [ 102 ] ( Fig. 3 ) ( Table 1 ).…”

The role of long noncoding RNAs in ocular angiogenesis and vascular oculopathy

“…In a streptozotocin (STZ)-induced diabetes model, about 303 lncRNAs were aberrantly expressed in the retinas of early DR, including 89 upregulated and 214 downregulated lncRNAs [ 48 ]. Among them, KCNQ1OT1 is upregulated in aqueous humor and serum samples of DR patients compared to normal subjects, as well as in human retinal ECs (hRECs) cultured in high glucose (HG) conditions [ 49 ]. HEIH is highly expressed both in the serum of diabetic subjects with DR and in ARPE-19 cells treated with HG conditions [ 50 , 51 ].…”