NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease

ABSTRACTObjective High expression of nuclear factor interleukin-3 (NFIL3) and integrin Alpha M (ITGAM) was found in serum samples from Kawasaki disease (KD) patients through bioinformatics analysis. Hence, this study aimed to explore the biological functions of NFIL3 and ITGAM in KD serum-stimulated...

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Main Authors: Li Chen, Zhiyang Shangguan, Zeya Dong, Qunfan Deng, Yunyun Ding, Shulong Yang
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:Hematology
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/16078454.2023.2277502
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author Li Chen
Zhiyang Shangguan
Zeya Dong
Qunfan Deng
Yunyun Ding
Shulong Yang
author_facet Li Chen
Zhiyang Shangguan
Zeya Dong
Qunfan Deng
Yunyun Ding
Shulong Yang
author_sort Li Chen
collection DOAJ
description ABSTRACTObjective High expression of nuclear factor interleukin-3 (NFIL3) and integrin Alpha M (ITGAM) was found in serum samples from Kawasaki disease (KD) patients through bioinformatics analysis. Hence, this study aimed to explore the biological functions of NFIL3 and ITGAM in KD serum-stimulated human coronary artery endothelial cells (HCAECs).Methods The differentially-expressed genes in KD were analyzed through bioinformatics analysis. Serum samples were obtained from 18 KD patients and 18 healthy volunteers, followed by detection of NFIL3 and ITGAM levels in KD serum. After HCAECs were transfected with sh-NFIL3, sh-ITGAM, or sh-NFIL3 + oe-ITGAM and underwent 24-h KD serum stimulation, cell viability and apoptosis and the levels of inflammation-related factors were measured. The binding between NFIL3 and ITGAM was validated by dual-luciferase and chromatin immunoprecipitation (ChIP) assays.Results NFIL3 and ITGAM were up-regulated in serum from KD patients and KD serum-stimulated HCAECs. Down-regulation of NFIL3 or ITGAM inhibited KD serum-induced cell apoptosis and inflammatory response of HCAECs and promoted cell viability. Mechanistically, NFIL3 promoted ITGAM transcription level. Up-regulation of ITGAM reversed the improvement of NFIL3 down-regulation on KD serum-induced HCAEC injury.Conclusion NFIL3 aggravated KD serum-induced HCAEC injury by promoting ITGAM transcription, which provided new insights into the treatment of KD.
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spelling doaj.art-41dbd0d439a6410fa6ad77b524614fb02023-11-07T13:21:25ZengTaylor & Francis GroupHematology1607-84542023-12-0128110.1080/16078454.2023.2277502NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki diseaseLi Chen0Zhiyang Shangguan1Zeya Dong2Qunfan Deng3Yunyun Ding4Shulong Yang5Clinical College, Fuzhou Medical College, Nanchang University, Fuzhou, People’s Republic of ChinaBasic Medicine College, Fuzhou Medical College, Nanchang University, Fuzhou, People’s Republic of ChinaClinical College, Fuzhou Medical College, Nanchang University, Fuzhou, People’s Republic of ChinaDepartment of Pediatrics, First People’s Hospital of Fuzhou, Fuzhou, People’s Republic of ChinaDepartment of Pediatrics, First People’s Hospital of Fuzhou, Fuzhou, People’s Republic of ChinaDepartment of Physiology, Fuzhou Medical College of Nanchang University, Fuzhou, People’s Republic of ChinaABSTRACTObjective High expression of nuclear factor interleukin-3 (NFIL3) and integrin Alpha M (ITGAM) was found in serum samples from Kawasaki disease (KD) patients through bioinformatics analysis. Hence, this study aimed to explore the biological functions of NFIL3 and ITGAM in KD serum-stimulated human coronary artery endothelial cells (HCAECs).Methods The differentially-expressed genes in KD were analyzed through bioinformatics analysis. Serum samples were obtained from 18 KD patients and 18 healthy volunteers, followed by detection of NFIL3 and ITGAM levels in KD serum. After HCAECs were transfected with sh-NFIL3, sh-ITGAM, or sh-NFIL3 + oe-ITGAM and underwent 24-h KD serum stimulation, cell viability and apoptosis and the levels of inflammation-related factors were measured. The binding between NFIL3 and ITGAM was validated by dual-luciferase and chromatin immunoprecipitation (ChIP) assays.Results NFIL3 and ITGAM were up-regulated in serum from KD patients and KD serum-stimulated HCAECs. Down-regulation of NFIL3 or ITGAM inhibited KD serum-induced cell apoptosis and inflammatory response of HCAECs and promoted cell viability. Mechanistically, NFIL3 promoted ITGAM transcription level. Up-regulation of ITGAM reversed the improvement of NFIL3 down-regulation on KD serum-induced HCAEC injury.Conclusion NFIL3 aggravated KD serum-induced HCAEC injury by promoting ITGAM transcription, which provided new insights into the treatment of KD.https://www.tandfonline.com/doi/10.1080/16078454.2023.2277502Human coronary artery endothelial cellsITGAMinflammationKawasaki diseaseNFIL3
spellingShingle Li Chen
Zhiyang Shangguan
Zeya Dong
Qunfan Deng
Yunyun Ding
Shulong Yang
NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease
Hematology
Human coronary artery endothelial cells
ITGAM
inflammation
Kawasaki disease
NFIL3
title NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease
title_full NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease
title_fullStr NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease
title_full_unstemmed NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease
title_short NFIL3 aggravates human coronary artery endothelial cell injury by promoting ITGAM transcription in Kawasaki disease
title_sort nfil3 aggravates human coronary artery endothelial cell injury by promoting itgam transcription in kawasaki disease
topic Human coronary artery endothelial cells
ITGAM
inflammation
Kawasaki disease
NFIL3
url https://www.tandfonline.com/doi/10.1080/16078454.2023.2277502
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