LncRNA GAS5 regulates angiogenesis by targeting miR‑10a‑3p/VEGFA in osteoporosis.

Abstract

Osteoporosis is a severe bone disease commonly occurring in older males and postmenopausal females. Previous studies have shown that long non‑coding (lnc)RNA growth arrest‑specific5 (GAS5) serves an important role in osteoporosis. However, its role is unclear and requires further exploration. The relative expression levels of GAS5 and miR‑10a‑3p in the serum samples of patients with osteoporosis, as well as the relative expression levels of GAS5, microRNA (miR)‑10a‑3p and vascular endothelial growth factorA (VEGFA) mRNA in osteoblasts, were detected by reverse transcription‑quantitative PCR. ELISA and western blotting were used to detect the expression levels of VEGFA. A Matrigel angiogenesis test was used to assess the effects on angiogenesis. RNA binding interactions between GAS5/miR‑10a‑3p and miR‑10a‑3p/VEGFA were evaluated using dual‑luciferase reporter assays. Furthermore, the effects of the GAS5/miR‑10a‑3p/VEGFA axis were investigated via ELISA, western blotting and Matrigel angiogenesis. GAS5 was significantly downregulated and miR‑10a‑3p was upregulated in patients with osteoporosis. Overexpression of GAS5 promoted angiogenesis. GAS5 acted as a sponge of miR‑10a‑3p; VEGFA was a target gene of miR‑10a‑3p. GAS5 induced angiogenesis by inhibiting miR‑10a‑3p and enhancing VEGFA expression. These results indicated that GAS5 overexpression increased angiogenesis by inhibiting miR‑10a‑3p, promoting the expression of VEGFA. The present study revealed a novel mechanism and provided novel targets for the clinical treatment of osteoporosis.