Kawasaki disease: SOCS2-AS1/miR-324-5p/CUEDC2 axis regulates the progression of human umbilical vein endothelial cells.
Abstract
Kawasaki disease (KD) is the most prevailing cause of acquired heart disease in children, due to permanent coronary artery damage. Recently, the role of long noncoding RNAs (lncRNAs) in human diseases has been highlighted. However, the role of lncRNA SOCS2 antisense RNA 1 (SOCS2-AS1) on the function of human umbilical vein endothelial cells (HUVECs) in KD remains elusive. SOCS2-AS1 expression was examined via RT-qPCR. CCK-8, EdU, caspase-3 activity, flow cytometry and TUNEL assays were conducted for exploring the function of SOCS2-AS1 in HUVECs of KD. The interaction among RNAs (SOCS2-AS1, miR-324-5p and CUEDC2) was validated via luciferase reporter, RIP and RNA pull-down assays. SOCS2-AS1 was highly expressed in serum and tissues of KD patients. SOCS2-AS1 depletion repressed the proliferation of HUVECs, whereas it facilitated apoptosis. Further, SOCS2-AS1 could bind with miR-324-5p and negatively regulated miR-324-5p expression in HUVECs. Besides, CUE domain containing 2 (CUEDC2) was the downstream target of miR-324-5p, and SOCS2-AS1 could release CUEDC2 expression via sponging miR-324-5p in HUVECs. Furthermore, downregulating miR-324-5p or upregulating CUEDC2 could rescue the progression of HUVECs restrained by SOCS2-AS1 knoc...Continue Reading
References
MicroRNA hsa-miR-324-5p Suppresses H5N1 Virus Replication by Targeting the Viral PB1 and Host CUEDC2
MiR-324-5p reduces viability and induces apoptosis in gastric cancer cells through modulating TSPAN8
Over-expression of miR-34a induces rapid cognitive impairment and Alzheimer's disease-like pathology
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Apoptosis
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis