ArticlePediatric research2022
Kawasaki disease: SOCS2-AS1/miR-324-5p/CUEDC2 axis regulates the progression of human umbilical vein endothelial cells.
Article in Pediatric research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 13 citations in OpenAlex.
- The role of microRNAs in Kawasaki disease: a systematic review.European journal of pediatrics · 2026Pooled it
- Role of long non-coding RNAs and circular RNAs in kawasaki disease: a systematic review.Pediatric rheumatology online journal · 2025Pooled it
- LncRNAs in Kawasaki disease and Henoch-Schönlein purpura: mechanisms and clinical applications.Molecular and cellular biochemistry · 2024Review
- Kawasaki disease: lncRNA Slco4a1 regulates the progression of human umbilical vein endothelial cells by targeting the miR-335-5p/POU5F1 axis.Translational pediatrics · 2022Article
- LncRNA FENDRR Servers as a Possible Marker of Essential Hypertension and Regulates Human Umbilical Vein Endothelial Cells Dysfunction via miR-423-5p/Nox4 Axis.International journal of general medicine · 2022Article
- Molecular mechanisms of endothelial dysfunction in Kawasaki-disease-associated vasculitis.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKawasaki 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.
methodsSOCS2-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.
resultsSOCS2-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.
conclusionsSOCS2-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.
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