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

Chen, Li; Shangguan, Zhiyang; Dong, Zeya; Deng, Qunfan; Ding, Yunyun; Yang, Shulong

doi:10.1080/16078454.2023.2277502

Hematology

2023

DOI: 10.1080/16078454.2023.2277502

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

Li Chen,

Zhiyang Shangguan,

Zeya Dong

et al.

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2024

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Knockdown of NFIL3 modulates the AMPK pathway to suppress excessive cell proliferation, inflammation, and migration in rheumatoid arthritis

Qiang,

Xuan,

Liu

et al. 2024

Int J of Rheum Dis

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BackgroundRheumatoid arthritis (RA) is one autoimmune disease that badly influences the lives of humans. Nuclear factor interleukin 3 (NFIL3) has been elucidated to join into the progression of diversiform diseases. According to a recent report, NFIL3 expression levels are increased in the peripheral blood and synovial tissues of individuals with RA. However, the detailed regulatory impacts of NFIL3 and associated pathways in RA progression need more investigations.MethodsThe mRNA and protein expressions were tested through RT‐qPCR and western blot. The cell proliferation was evaluated through CCK‐8 and EdU assay. The cell apoptosis was measured through flow cytometry. The levels of TNF‐α, IL‐6, and IL‐8 were assessed through ELISA. The cell migration and invasion were tested through Transwell assay.ResultsIn this study, NFIL3 exhibited higher expression in RA fibroblast‐like synoviocytes (interleukin‐1β [IL‐1β]‐triggered MH7A cell model). In addition, knockdown of NFIL3 repressed the growth of IL‐1β‐mediated MH7A cells. It was also demonstrated that suppressing NFIL3 resulted in reduced inflammatory reactions in IL‐1β‐mediated MH7A cells. Suppression of NFIL3 alleviated cell migration and invasion in the RA cell model. Ultimately, it was demonstrated that NFIL3 retarded the AMPK/mTOR pathway.ConclusionThis study demonstrated that the inhibition of NFIL3 effectively controlled the AMPK/mTOR pathway, thereby suppressing the overactive proliferation, inflammation, and migration of fibroblast‐like synoviocytes in human RA. This discovery implied that NFIL3 can be a serviceable biomarker for RA therapy.

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Knockdown of NFIL3 modulates the AMPK pathway to suppress excessive cell proliferation, inflammation, and migration in rheumatoid arthritis

Qiang,

Xuan,

Liu

et al. 2024

Int J of Rheum Dis

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

Cited by 1 publication

References 33 publications

Knockdown of NFIL3 modulates the AMPK pathway to suppress excessive cell proliferation, inflammation, and migration in rheumatoid arthritis

Knockdown of NFIL3 modulates the AMPK pathway to suppress excessive cell proliferation, inflammation, and migration in rheumatoid arthritis

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