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

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 FO...

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Veröffentlicht in:Immunity, Inflammation and Disease Inflammation and Disease, 2023-07, Vol.11 (7), p.e939-n/a
Hauptverfasser: Zheng, Ronghao, Xie, Jing, Li, Weijie, Shang, Jianping, Shi, Zuliang, Zhu, Songbai, Gui, Lin, Huang, Li, Shu, Lan, Liu, Donglei, Gong, Yi, Li, Xiaohui, Chai, Wanxia, Huang, Xiaofen, Wu, Xiaolin, Yue, Jing
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Sprache:eng
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Zusammenfassung: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. Overexpression of miR‐223‐3p also promoted the apoptosis of HCAECs. In addition, serum from KD patients promoted apoptosis, whereas serum after IVIG treatment inhibited apoptosis. KD patient serum downregulated the expression of FOXP3, Bcl2, TGF‐β1 and IL‐10 in cells, and upregulated the expression of caspase3, Bax, IL‐17, IL‐6, and IL‐23. The opposite results were obtained with IVIG‐treated sera. Conclusion miR‐223‐3p secreted in serum of KD patients can regulate the expression of FOXP3 and affect the proliferation, apoptosis, and inflammation of cells. It was verified that Kawasaki disease (KD) serum has high level of miR‐223‐3p and low level of FOXP3. A co‐culture system was established with HCAECs cells and THP1 cells treated with three serum samples. It was verified that serum miR‐223‐3p in KD patients may affect cell proliferation, apoptosis, the expression of inflammatory cytokines, and the level of angiogenesis factors by regulating FOXP3.
ISSN:2050-4527
2050-4527
DOI:10.1002/iid3.939