Bone Marrow–Derived MicroRNA‐223 Works as an Endocrine Genetic Signal in Vascular Endothelial Cells and Participates in Vascular Injury From Kawasaki Disease

Chu, Maoping; Wu, Rongzhou; Qin, Shanshan; Hua, Wenfeng; Zhang, Shan; Rong, Xing; Zeng, Jingjing; Hong, Lanlan; Sun, Yeying; Liu, Ying; Li, Wen; Wang, Shenming; Zhang, Chunxiang

doi:10.1161/jaha.116.004878

Cited by 53 publications

(57 citation statements)

References 27 publications

(93 reference statements)

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“…Recently, one research showed that, the mechanism of miRNA-involved blood vessel damage, particularly the protective mechanism, remains unclear. One research showed that KD-induced endothelial cell apoptotic could be inhibited by knockdown of miR-223, which was up-regulated in KD serum [3]. In addition, Another study showed that miR-125a-5p increased in plasma induced endothelial cell apoptotic [29].…”

Section: Discussionmentioning

confidence: 99%

“…We previously revealed that many miRNAs, including miR-27b, are differentially expressed in serum from KD patients compared with healthy children [3]. However, the functions of these miRNAs in KD are not clear.…”

Section: Mir-27b Is Increased In Kd Serum and Mir-27b Levels In Serummentioning

confidence: 99%

“…Many studies showed that the increase of miRNA expression in the blood can cause the increase of expression in the endothelial cells and thus affect the function of endothelial cells [3,11]. In order to investigate whether KD serum can increase the expression of miR27b in endothelial cells and the function of upregulation of miR27b in KD serum, we performed the following experiments.…”

Section: Upregulation Of Mir-27b Inhibits the Proliferation And Migramentioning

confidence: 99%

“…KD is the most common cause of coronary artery aneurysms (CAAs) in childhood. Moreover, 15 to 25% of untreated children develop CAAs or ectasia [1] and the risk is reduced only to 5% after treatment with intravenous immunoglobin in acute KD [2,3]. However, the mechanism of KD-induced vascular injury remains unclear and no specific biomarker is available.…”

Section: Introductionmentioning

confidence: 99%

“…However, the mechanism of KD-induced vascular injury remains unclear and no specific biomarker is available. Chu et al indicated that miR-223 might participate in vascular injury in KD [3]. Using a KD mouse model, interleukin (IL)-1β and caspase-1 were determined to be critical for Lactobacillus casei wall extract-mediated coronary arteritis.…”

Section: Introductionmentioning

confidence: 99%

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miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease

Rong

Shen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidence indicates that microRNAs (miRNAs) play important roles in Kawasaki disease (KD). Our previous study demonstrated that hsa-miR-27b-3p (miR-27b) was up-regulated in KD serum. However, the specific role of miR-27b in KD remains unclear. We aimed to investigate that miR-27b could be a biomarker and therapeutic target for KD treatment. As well, the specific mechanism of miR-27b effecting endothelial cell functions was studied. Methods: The expression of miR-27b and Smad7 was measured by qRT-PCR. Gain-of-function strategy was used to observe the effect of miR-27b on human umbilical vein endothelial cells (HUVECs) proliferation and migration. Bioinformatics analyses were applied to predict miR-27b targets and then we verified Smad7 by a luciferase reporter assay. Western blot was performed to detect the protein expression of Smad7, PCNA, MMP9, MMP12 and TGF-β-related genes. Results: We confirmed that miR-27b was shown to be dramatically up-regulated in KD serum and KD serum-treated HUVECs and that elevated expression of miR-27b suppressed the proliferation and migration of HUVECs. Furthermore, our results verified that miR-27b mediated cell functions by affecting the TGF-β via targeting Smad7 in HUVECs. Conclusion: These results suggested that up-regulated miR-27b had a protective role in HUVECs proliferation and migration via targeting Smad7 and affecting TGF-β pathway. Therefore, miR-27b represented a potential biomarker for KD and may serve as a promising therapeutic target for KD treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Mir-27b Is Increased In Kd Serum and Mir-27b Levels In Serummentioning

confidence: 99%

Section: Upregulation Of Mir-27b Inhibits the Proliferation And Migramentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease

Rong

Shen

et al. 2018

Cell Physiol Biochem

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Non‐coding RNAs in Kawasaki disease: Molecular mechanisms and clinical implications

Yang

Ding

et al. 2022

BioEssays

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Kawasaki disease (KD) is an acute self-limiting vasculitis with coronary complications, usually occurring in children. The incidence of KD in children is increasing year by year, mainly in East Asian countries, but relatively stably in Europe and America. Although studies on KD have been reported, the pathogenesis of KD is unknown. With the development of high-throughput sequencing technology, growing number of regulatory noncoding RNAs (ncRNAs) including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA) have been identified to involved in KD. However, the role of ncRNAs in KD has not been comprehensively elucidated. Therefore, it is significative to study the regulatory role of ncRNA in KD, which might help to uncover new and effective therapeutic strategies for KD. In this review, we summarize recent studies on ncRNA in KD from the perspectives of immune disorders, inflammatory disorders, and endothelial dysfunction, and highlight the potential of ncRNAs as therapeutic targets for KD.

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MiR‐223‐3p affects the proliferation and apoptosis of HCAECs in Kawasaki disease by regulating the expression of FOXP3

Zheng

Xie

et al. 2023

Immunity Inflam & Disease

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Objective: Kawasaki disease (KD) can lead to permanent damage to coronary structures, the pathogenesis of which remains unknown. This experiment was designed to investigate whether miR-223-3p secreted in the serum of KD patients affects the proliferation and apoptosis of HCAECs in KD by regulating FOXP3.Methods: Blood samples were collected in acute febrile phase of KD, after IVIG treatment, and from healthy controls. Transfected into HCAECs cells by synthetic FOXP3 siRNA/NC. A co-culture system was established between HCAECs cells transfected with FOXP3 siRNA/NC and THP1 cells added with three sera. Results: Compared with the control group, the expressions of miR-223-3p, RORγt, and Th17 in serum of KD patients were significantly upregulated, and the expressions of TGF-β1, FOXP3 and Treg were significantly downregulated. At the same time, the levels of IL-6, IL-17, and IL-23 were significantly increased, and the levels of IL-10 and FOXP3 were significantly decreased. After IVIG treatment, the patient's above results were reversed. The serum of KD patients increased the expression of miR-223-3p and inhibited the expression of FOXP3 in HCAECs cells. IVIG serum is the opposite.

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Bone Marrow–Derived MicroRNA‐223 Works as an Endocrine Genetic Signal in Vascular Endothelial Cells and Participates in Vascular Injury From Kawasaki Disease

Cited by 53 publications

References 27 publications

miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease

miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease

Non‐coding RNAs in Kawasaki disease: Molecular mechanisms and clinical implications

MiR‐223‐3p affects the proliferation and apoptosis of HCAECs in Kawasaki disease by regulating the expression of FOXP3

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