Kaohsiung Journal of Medical Sciences (Jan 2023)
LncRNA SNHG1 targets miR‐340‐5p/PIK3CA axis to regulate microvascular endothelial cell proliferation, migration, and angiogenesis in DR
Abstract
Abstract Diabetic retinopathy (DR) is a serious long‐term complication of diabetes. However, the current treatment of DR is still challenging. We aimed to investigate the role of lncRNA SNHG1/miR‐340‐5p/PIK3CA in DR and the mechanisms involved. Blood samples from clinical DR patients and healthy subjects were obtained. HRMECs were induced by high glucose for 24 h to establish the DR model. The vector for interfering or overexpressing lncRNA SNHG1, miR‐340‐5p, and PIK3CA was constructed. LncRNA SNHG1, miR‐340‐5p, and PIK3CA expressions were detected by qRT‐PCR or Western blot. Cell proliferation and migration were detected by CCK‐8 and Transwell assays. Blood vessel formation was detected by angiogenesis assay. Dual‐luciferase reporter assay tested the interaction of lncRNA SNHG1 with miR‐340‐5p and miR‐340‐5p with PIK3CA. RIP measured the binding of miR‐340‐5p to PIK3CA. In the blood of DR patients and the DR model, lncRNA SNHG1 was increased and miR‐340‐5p expression was down‐regulated. In the DR model, PIK3CA expression was elevated. Downregulation of lncRNA SNHG1 inhibited HRMECs proliferation, migration, and angiogenesis. LncRNA SNHG1 interacted with miR‐340‐5p, and up‐regulation of miR‐340‐5p inhibited HRMECs proliferation, migration and angiogenesis. The inhibition of cell proliferation, migration, and angiogenesis of HRMECs caused by down‐regulation of lncRNA SNHG1 was reversed by knockdown of miR‐340‐5p. miR‐340‐5p targeted PIK3CA, and downregulation of PIK3CA inhibited HRMECs proliferation, migration, and angiogenesis. The inhibition of HRMECs proliferation, migration and angiogenesis caused by down‐regulation of lncRNA SNHG1 could be reversed by overexpression of PIK3CA. LncRNA SNHG1 targeted miR‐340‐5p/PIK3CA axis to regulate microvascular endothelial cell proliferation, migration, and angiogenesis in DR.
Keywords