Silencing long non-coding RNA SNHG3 repairs the dysfunction of pulmonary microvascular endothelial barrier by regulating miR-186-5p/Wnt axis

• DOI: 10.1016/j.bbrc.2022.11.067
• Publication Date: 2022-11-24T20:30:30Z
• Authors: Yanli Wu; Mei Li; Jijia Bai; Xigang Ma
• Keywords: Barrier function

Barrier permeability changes of human pulmonary microvascular endothelial cells (HPMVECs) are important in sepsis-related acute lung injury (ALI) pathogenesis. Long non-coding small nucleolar RNA host gene 3 (SNHG3) mediates the cell-biological phenotype cancer and affects progression cancer, but its role regulating functions non-malignant is still rarely reported. Therefore, we evaluated regulatory effect SNHG3 on function PMVECs ALI. Small interference (siRNA)-mediated deletion promoted proliferation PMVECs, reduced apoptosis barrier permeability, increased expression tight junction proteins claudin-5 ZO-1. Knockdown miR-186-5p expression, while overexpression upregulated level wnt5a. Through a dual luciferase reporter assay, confirmed binding between miR-186-5p, We further found that knockout could inhibit cell proliferation, increase down-regulate Importantly, silencing activating Wnt signal pathway eliminate repair caused by down-regulation SNHG3. To sum up, our results suggested knockdown long repaired dysfunction through miR-186-5p/Wnt axis.