Jing Zhao1, Daye Chen2. 1. Department of Pediatrics, Yancheng Maternal and Child Health Care Hospital, Yancheng, Jiangsu, 224002, China. 2. Department of Pediatrics, Wuxi Xishan District People's Hospital, Zhongda Hospital Wuxi Branch, Southeast University, Wuxi, Jiangsu, 214101, China. chenyong6638851@163.com.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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 knockdown. CONCLUSIONS: SOCS2-AS1 upregulates CUEDC2 via inhibiting miR-324-5p to promote the progression of HUVECs in KD, providing new insights for KD treatment. IMPACT: SOCS2-AS1 is highly expressed in the serum of KD patients. SOCS2-AS1 contributes to cell proliferation in HUVECs of KD through elevating CUEDC2 expression by sequestering miR-324-5p. SOCS2-AS1/miR-324-5p/CUEDC2 axis exerts a progression-facilitating function in KD. These findings suggest SOCS2-AS1 as a novel potential target for KD treatment.
BACKGROUND: 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. METHODS: 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. RESULTS: 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 knockdown. CONCLUSIONS: SOCS2-AS1 upregulates CUEDC2 via inhibiting miR-324-5p to promote the progression of HUVECs in KD, providing new insights for KD treatment. IMPACT: SOCS2-AS1 is highly expressed in the serum of KD patients. SOCS2-AS1 contributes to cell proliferation in HUVECs of KD through elevating CUEDC2 expression by sequestering miR-324-5p. SOCS2-AS1/miR-324-5p/CUEDC2 axis exerts a progression-facilitating function in KD. These findings suggest SOCS2-AS1 as a novel potential target for KD treatment.
Authors: Mohsen Yari; Sara Bitarafan; Mohammad Ali Broumand; Zahra Fazeli; Mahnoosh Rahimi; Sayyed Mohammad Hossein Ghaderian; Reza Mirfakhraie; Mir Davood Omrani Journal: Int J Mol Cell Med Date: 2018-02-10