Kawasaki disease: SOCS2-AS1/miR-324-5p/CUEDC2 axis regulates the progression of human umbilical vein endothelial cells

Zhao, Jing; Chen, Daye

doi:10.1038/s41390-020-1029-9

Cited by 13 publications

(20 citation statements)

References 33 publications

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“…Moreover, a recent study has revealed that the lncRNA SOCS2 and its antisense RNA AS1 were highly expressed in the serum of patients with KD, and they contributed to cell proliferation in the human umbilical vein endothelial cells of patients with KD by elevating CUEDC2 expression by sequestering miR-324-5p. 38 Compared with those studies, this study adopted a different analysis method as CAGE-seq was employed to analyze gene expression. In addition, monocytes, which were key players of innate immunity, were analyzed because they initially appeared during the acute phase of KD.…”

Section: Discussionmentioning

confidence: 99%

G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1

et al. 2022

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Background Kawasaki disease (KD) is a systemic vasculitis that is currently the most common cause of acquired heart disease in children. However, its etiology remains unknown. Long non-coding RNAs (lncRNAs) contribute to the pathophysiology of various diseases. Few studies have reported the role of lncRNAs in KD inflammation; thus, we investigated the role of lncRNA in KD inflammation. Methods A total of 50 patients with KD (median age, 19 months; 29 males and 21 females) were enrolled. We conducted cap analysis gene expression sequencing to determine differentially expressed genes in monocytes of the peripheral blood of the subjects. Results About 21 candidate lncRNA transcripts were identified. The analyses of transcriptome and gene ontology revealed that the immune system was involved in KD. Among these genes, G0/G1 switch gene 2 (G0S2) and its antisense lncRNA, HSD11B1-AS1, were upregulated during the acute phase of KD ( P < 0.0001 and <0.0001, respectively). Moreover, G0S2 increased when lipopolysaccharides induced inflammation in THP-1 monocytes, and silencing of G0S2 suppressed the expression of HSD11B1-AS1 and tumor necrosis factor-α. Conclusions This study uncovered the crucial role of lncRNAs in innate immunity in acute KD. LncRNA may be a novel target for the diagnosis of KD. Impact This study revealed the whole aspect of the gene expression profile of monocytes of patients with Kawasaki disease (KD) using cap analysis gene expression sequencing and identified KD-specific molecules: G0/G1 switch gene 2 (G0S2) and long non-coding RNA (lncRNA) HSD11B1-AS1. We demonstrated that G0S2 and its antisense HSD11B1-AS1 were associated with inflammation of innate immunity in KD. lncRNA may be a novel key target for the diagnosis of patients with KD.

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Section: Discussionmentioning

confidence: 99%

G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1

et al. 2022

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“…Jiang et al (9) have reported that high expression of lncRNA PINC promotes apoptosis of vascular endothelial cells, suggesting that inhibition of lncRNA PINC may contribute to the prevention and treatment of KD. Zhao et al (8) found that lncRNA SOCS2-AS1 up-regulated CUEDC2 by inhibiting miR-324-5p and promoted the progress of HUVECs in KD, providing new insights for KD treatment. However, the identities and putative functions of lncRNA transcripts in KD remain elusive.…”

Section: Discussionmentioning

confidence: 99%

“…The hypotheses regarding the molecular mechanisms of KD are listed as follows: inflammatory factors involved in coronary artery injury and remodeling, molecular abnormalities in immune signal transduction pathways, endothelium injury, and metabolic disorders of the cell matrix, among others (4)(5)(6). In addition, some researchers have shown that long non-coding RNAs (lncRNAs) may be involved in the progression of KD by regulating their targets (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Kawasaki disease: lncRNA Slco4a1 regulates the progression of human umbilical vein endothelial cells by targeting the miR-335-5p/POU5F1 axis

Hao¹,

Zhang²,

Pan³

et al. 2022

Transl Pediatr

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Background: Kawasaki disease (KD) is an autoimmune disease with systemic vasculitis as the main pathological change, and is most common in children under 5. The role of long non-coding RNAs (lncRNAs) in human diseases has been highlighted. LncRNA Slco4a1 was reported to promote cell growth and act as an oncogenic regulator in cancer. However, the role of lncRNA Slco4a1 in KD remains unclear. This study aimed to investigate the role and mechanism of lncRNA Slco4a1 in KD.Methods: Enzyme linked immunosorbent assay (ELISA), qRT-PCR, Western blot, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining were conducted to explore the function of lncRNA Slco4a1. The interaction between POU5F1 and miR-335-5p was analyzed by the RIP assay and dual luciferase assay.Results: LncRNA Slco4a1 was significantly upregulated in the serum of KD patients compared with healthy controls. LncRNA Slco4a1 was upregulated in human umbilical vein endothelial cells (HUVECs) stimulated with KD serum. LncRNA Slco4a1 overexpression could promote the expression of inflammatory factors and apoptosis in HUVECs. The number of inflammatory cells and the infiltration area of the coronary artery in KD rats were decreased after lncRNA Slco4a1 silencing. Furthermore, lncRNA Slco4a1 is a sponge of miR-335-5p and negatively regulated the expression of miR-335-5p. POU5F1 was the downstream target of miR-335-5p, and miR-335-5p overexpression could upregulate the expression of POU5F1. Additionally, miR-335-5p overexpression could inhibit the expression of inflammatory factors and apoptosis in HUVECs. We further investigated the effect of lncRNA Slco4a1 on the mitogen-activated protein kinase (MAPK) signaling pathway, and the results showed that lncRNA Slco4a1 could promote the activation of the MAPK signaling pathway.Conclusions: Together, these results indicated that lncRNA Slco4a1 could regulate the progression of HUVECs in KD by targeting the miR-335-5p/POU5F1 axis, providing new insights for KD treatment.

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“… 31 Incidentally, an illustration about patients with Kawasaki disease pinpoints the knockdown of lncRNA SOCS2-AS1 encourages the apoptotic HUVECs and accommodates the proliferation of HUVECs by controlling the miR-423-5p/ CUEDC2 axis. 32 The overexpression of FENDRR appearance expansionary effect on apoptosis of microvascular endothelial cells. 11 Hypertension is closely related to reduced endothelial homeostasis.…”

Section: Discussionmentioning

confidence: 99%

LncRNA FENDRR Servers as a Possible Marker of Essential Hypertension and Regulates Human Umbilical Vein Endothelial Cells Dysfunction via miR-423-5p/Nox4 Axis

Zhao¹,

Wang²,

Liu³

et al. 2022

IJGM

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Purpose Essential hypertension (EH) is an intricate non-communicable infirmity and lncRNAs are validated as essential mediators in EH. The study aimed to propose the expression pattern of FENDRR and miR-423-5p, substantiate the potential mechanism of FENDRR/miR-423-5p/Nox4 axis in EH. Patients and Methods The expression of FENDRR and miR-423-5p was evaluated by qRT-PCR and the clinical significance was explored by the ROC curve. Pearson correlation indicated the relationship between FENDRR and miR-423-5p. The function of FENDRR and miR-423-5p on HUVECs was clarified by CCK-8 assay, Transwell assay, and flow cytometry. Western blot was used to assess the relative protein expression of Nox4. Results FENDRR was highly expressed and miR-423-5p was lowly expressed in EH patients and a negative correlation between them was determined. FENDRR might serve as a predictive diagnosis in differentiating EH patients. Knockdown of FENDRR or overexpression of miR-423-5p showed expansionary effects in cell proliferation, cell migration, and inhibiting cell apoptosis. Meanwhile, miR-423-5p was determined as a target of FENDRR and mediated the function of FENDRR on HUVECs. Moreover, Nox4 is a down-streaming target gene of miR-423-5p. The protein expression of Nox4 was regulated by the alternation of miR-423-5p expression. Conclusion FENDRR played an energetic role in EH and contributed to HUVECs dysfunction by restricting cell proliferation, suppressing cell migration, and accelerating cell apoptosis by manipulating the miR-423-5p/Nox4 axis.

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Kawasaki disease: SOCS2-AS1/miR-324-5p/CUEDC2 axis regulates the progression of human umbilical vein endothelial cells

Cited by 13 publications

References 33 publications

G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1

G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1

Kawasaki disease: lncRNA Slco4a1 regulates the progression of human umbilical vein endothelial cells by targeting the miR-335-5p/POU5F1 axis

LncRNA FENDRR Servers as a Possible Marker of Essential Hypertension and Regulates Human Umbilical Vein Endothelial Cells Dysfunction via miR-423-5p/Nox4 Axis

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