lncRNA GAS5 regulates angiogenesis by targeting miR-10a-3p/VEGFA in osteoporosis

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-specific 5 (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 factor A (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.