Affiliations: [a]
Department of Ophthalmology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China
| [b]
Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China
Correspondence:
[*]
Corresponding authors: Qi Zhou and Hongbin Lv, The Affiliated Hospital of Southwest Medical University, No.25 Taiping Street, Jiangyang District, Luzhou, Sichuan, 646000, China. E-mails: zhouqi051@swmu.edu.cn (Qi Zhou) and oculistlvhongbin@swmu.edu.cn (Hongbin Lv).
Abstract: PURPOSE:Diabetic retinopathy (DR) is a serious retinal vascular disease that affects many individuals in their prime working years. The present research aimed at whether and how LOC681216 (LNC-216) is involved in retinal vascular dysfunction under diabetic conditions. METHODS:Rat retinal microvascular endothelial cells (RRMECs) treated with high glucose (HG) were used for functional analysis. Gene expression analysis was conducted using the Clariom D Affymetrix platform. The wound healing, transwell, and vascular tube formation assays were used to identify the migration, invasion, and tube formation capability of RRMECs. The dual-luciferase reporter confirmed the binding interaction between miR-143-5p and LNC-216 or matrix metallopeptidase 2 (MMP2). RESULTS:Lnc-216 was upregulated in RRMECs treated with HG. Lnc-216 knockdown markedly suppressed the tube formation, cell migration, and wound healing of cultured RRMECs under HG conditions. Mechanistically, Lnc-216 acted as a miR-143-5p sponge to affect the biological activity of miR-143-5p, which led to increased expression of matrix metallopeptidase 2 (MMP2). CONCLUSIONS:Lnc-216 attenuates diabetic retinal vascular dysfunction through the miR-143-5p/MMP2 axis, providing a potential therapeutic strategy for DR.
