{Reference Type}: Journal Article
{Title}: Lnc-216 regulates the miR-143-5p /MMP2 signaling axis aggravates retinal endothelial cell dysfunction.
{Author}: Wang F;Guo Z;Yang G;Yang F;Zhou Q;Lv H;
{Journal}: Clin Hemorheol Microcirc
{Volume}: 0
{Issue}: 0
{Year}: 2024 Jun 27
{Factor}: 2.411
{DOI}: 10.3233/CH-242163
{Abstract}: <B>UNASSIGNED: </B>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.<BR><B>UNASSIGNED: </B>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).<BR><B>UNASSIGNED: </B>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).<BR><B>UNASSIGNED: </B>Lnc-216 attenuates diabetic retinal vascular dysfunction through the miR-143-5p/MMP2 axis, providing a potential therapeutic strategy for DR.