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Fibroblast growth factor 22 is a novel modulator of depression through interleukin-1?.

ABSTRACT: BACKGROUND AND AIMS:Emerging evidence shows that fibroblast growth factor 22 (FGF22) plays a critical role in the etiology of depression. However, the molecular mechanisms of FGF22 are not fully comprehended. Here, the effect of FGF22 in depression and its relationship with interleukin-1? (IL-1?) were investigated in clinical, animal, and cell experiments. METHODS:Serum from depressive patients was collected, and the levels of FGF22 and IL-1? were analyzed by ELISA. The chronic unpredictable mild stress (CUMS) model was established, and primary hippocampal neuronal cells were cultured to examine changes in FGF22 and IL-1? levels in rat hippocampus. RESULTS:The results revealed a negative correlation between serum FGF22 levels and serum IL-1? levels. The expression of IL-1? in the CUMS rat hippocampus decreased, and the apoptosis of hippocampal cells improved after the injection of lentiviral vector-mediated FGF22 (LV-FGF22). Further tests in primary hippocampal neuronal cells also showed a reduction in IL-1? and the cell apoptosis rate after treatment with FGF22. CONCLUSION:In conclusion, the results revealed that FGF22 plays a role in alleviating depression, which may be mediated by reduced expression of IL-1?.

SUBMITTER: Xu YH

PROVIDER: S-EPMC6492756 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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Fibroblast growth factor 22 is a novel modulator of depression through interleukin-1β.

Xu Yu-Hao YH Yu Ming M Wei Hong H Yao Shun S Chen Si-Yuan SY Zhu Xiao-Lan XL Li Yue-Feng YF

CNS neuroscience & therapeutics 20170925 11

<h4>Background and aims</h4>Emerging evidence shows that fibroblast growth factor 22 (FGF22) plays a critical role in the etiology of depression. However, the molecular mechanisms of FGF22 are not fully comprehended. Here, the effect of FGF22 in depression and its relationship with interleukin-1β (IL-1β) were investigated in clinical, animal, and cell experiments.<h4>Methods</h4>Serum from depressive patients was collected, and the levels of FGF22 and IL-1β were analyzed by ELISA. The chronic un ...[more]

PMID: 28948716

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Project description:The expression of granulocyte colony-stimulating factor (G-CSF), the major regulator of neutrophil maturation, by human fibroblast-like synoviocytes (FLS) can be stimulated by the inflammatory cytokine interleukin-1β (IL-1β). G-CSF is known to contribute to the pathologic processes of destructive arthritis, but the induction mechanism remains unknown. The aims of this study were to identify the signaling pathways involved in IL-1β-stimulated G-CSF production and to determine whether this process was inhibited by aciculatin (8-((2R,4S,5S,6R)-tetrahydro-4,5-dihydroxy-6-methyl-2H-pyran-2-yl)-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4H-chromen-4-one), the major bioactive component of Chrysopogon aciculatus. IL-1β-induced cytokine expression was evaluated by measuring mRNA and protein levels by RT-PCR, ELISA, and Milliplex® assay. Whether aciculatin inhibited IL-1β-stimulated G-CSF expression, and if so, how, were evaluated using western blot assay, an electrophoretic mobility shift assay, and a reporter gene assay. Neutrophil differentiation was determined by Wright-Giemsa staining and flow cytometry. Aciculatin markedly inhibited G-CSF expression induced by IL-1β (10 ng/mL) in a concentration-dependent manner (1-10 µM). In clarifying the mechanisms involved, aciculatin was found to inhibit the IL-1β-induced activation of the IκB kinase (IKK)/IκB/nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways by suppressing the DNA binding activity of the transcription factors NF-κB and activator protein (AP)-1. Furthermore, aciculatin significantly inhibited the G-CSF-mediated phosphorylation of Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Akt and neutrophil differentiation from precursor cells. Our results show that aciculatin inhibits IL-1β-stimulated G-CSF expression and the subsequent neutrophil differentiation, suggesting that it might have therapeutic potential for inflammatory arthritis.

Dataset Information

Fibroblast growth factor 22 is a novel modulator of depression through interleukin-1?.

Publications

Fibroblast growth factor 22 is a novel modulator of depression through interleukin-1β.

Similar Datasets

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