Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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).
UNASSIGNED: Lnc-216 attenuates diabetic retinal vascular dysfunction through the miR-143-5p/MMP2 axis, providing a potential therapeutic strategy for DR.
UNASSIGNED: 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).
UNASSIGNED: 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).
UNASSIGNED: Lnc-216 attenuates diabetic retinal vascular dysfunction through the miR-143-5p/MMP2 axis, providing a potential therapeutic strategy for DR.
摘要：
■糖尿病性视网膜病变（DR）是一种严重的视网膜血管疾病，影响许多人在其主要工作年限。本研究针对LOC681216（LNC-216）是否以及如何参与糖尿病条件下的视网膜血管功能障碍。
■用高葡萄糖(HG)处理的大鼠视网膜微血管内皮细胞(RRMEC)用于功能分析。使用ClariomDAffymetrix平台进行基因表达分析。伤口愈合，transwell,和血管形成测定用于识别迁移，入侵,和RRMEC的成管能力。双荧光素酶报告基因证实了miR-143-5p与LNC-216或基质金属肽酶2(MMP2)之间的结合相互作用。
■Lnc-216在用HG处理的RRMEC中上调。Lnc-216敲除明显抑制了管的形成，细胞迁移，和HG条件下培养的RRMEC的伤口愈合。机械上,Lnc-216作为miR-143-5p海绵影响miR-143-5p的生物学活性,这导致基质金属肽酶2（MMP2）的表达增加。
■Lnc-216通过miR-143-5p/MMP2轴减弱糖尿病视网膜血管功能障碍,为DR提供潜在的治疗策略。
■用高葡萄糖(HG)处理的大鼠视网膜微血管内皮细胞(RRMEC)用于功能分析。使用ClariomDAffymetrix平台进行基因表达分析。伤口愈合，transwell,和血管形成测定用于识别迁移，入侵,和RRMEC的成管能力。双荧光素酶报告基因证实了miR-143-5p与LNC-216或基质金属肽酶2(MMP2)之间的结合相互作用。
■Lnc-216在用HG处理的RRMEC中上调。Lnc-216敲除明显抑制了管的形成，细胞迁移，和HG条件下培养的RRMEC的伤口愈合。机械上,Lnc-216作为miR-143-5p海绵影响miR-143-5p的生物学活性,这导致基质金属肽酶2（MMP2）的表达增加。
■Lnc-216通过miR-143-5p/MMP2轴减弱糖尿病视网膜血管功能障碍,为DR提供潜在的治疗策略。
