Background: Rheumatoid 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.
Methods: The 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.
Results: In 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.
Conclusion: This 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.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/1756-185X.15287 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Circadian rhythm mechanisms underlying convergent adaptation of unihemispheric slow-wave sleep in marine mammals.
Mol Biol Evol
December 2024
Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, Guangdong 511458, China.
Marine mammals have evolved unihemispheric slow wave sleep (USWS), a unique state during which one cerebral hemisphere sleeps while the other remains awake, to mitigate the fundamental conflict between sleep and wakefulness. However, the underlying mechanisms remain largely unclear. Here, we use a comparative phylogenetic approach to analyze genes associated with light-dependent circadian mechanisms, aiming to reconstruct the evolution of the circadian rhythm pathway in mammals and to identify adaptively changed components likely to have contributed to the development of USWS.
View Article and Find Full Text PDFIntegrative multi-omics approach using random forest and artificial neural network models for early diagnosis and immune infiltration characterization in ischemic stroke.
Front Neurol
December 2024
Department of Neurology, Huizhou Hospital of Guangzhou University of Chinese Medicine (Huizhou Hospital of Traditional Chinese Medicine), Huizhou, Guangdong, China.
Article Synopsis
- Ischemic stroke (IS) is a major health concern worldwide, necessitating new diagnostic models due to limitations in existing methods.
- Using gene expression data from specific databases, researchers identified 26 differentially expressed genes (DEGs) and developed predictive models showing high accuracy in classifying IS.
- The findings highlight key DEGs and immune cell involvement in IS, suggesting their potential roles in understanding and treating the condition.
NFIL3/Tim3 axis regulates effector Th1 inflammation in COPD mice.
Front Immunol
November 2024
Wuming Hospital of Guangxi Medical University, Nanning, China.
Background: IFN-γ+CD4+ cells (type 1 helper T cells, Th1) represent a critical component of the inflammatory environment in the lungs of chronic obstructive pulmonary disease (COPD). Identifying influencing factors related to COPD-associated Th1 cells will enhance our understanding of the inflammatory mechanisms involved and facilitate the development of targeted interventions.
Method: We describe T-cell immunoglobulin and mucin-domain containing-3 (Tim3) as a key gene regulating COPD-associated Th1 cells through single-cell sequencing, flow cytometry and knockout mice.
OPN-Mediated Crosstalk Between Hepatocyte E4BP4 and Hepatic Stellate Cells Promotes MASH-Associated Liver Fibrosis.
Adv Sci (Weinh)
December 2024
Department of Molecular & Integrative Physiology, University of Michigan Medical School, NCRC 20-3843, 2800 Plymouth Road, Ann Arbor, MI, 48105, USA.
Stressed hepatocytes promote liver fibrosis through communications with hepatic stellate cells (HSCs) during chronic liver injury. However, intra-hepatocyte players that facilitate such cell-to-cell communications are largely undefined. It is previously reported that hepatocyte E4BP4 is potently induced by ER stress and hepatocyte deletion of E4bp4 protects mice from high-fat diet-induced liver steatosis.
View Article and Find Full Text PDFAnatomy of a superenhancer.
Adv Immunol
September 2024
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, United States. Electronic address:
Article Synopsis
- IRF8 is a key transcription factor that determines the development and function of specific immune cells, including dendritic cells and monocytes.
- The regulation of the Irf8 gene involves multiple enhancers that control its expression during different stages of cell development, each responding to specific transcription factors.
- Research shows that the activation of these enhancers is interdependent, meaning that each enhancer must be activated sequentially to properly regulate IRF8 expression and the formation of immune cell precursors.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!