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http://140.112.115.32:8080/ir/handle/987654321/1524
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| Title: | The mood stabilizer valproate activates human FGF1 gene promoter through inhibiting HDAC and GSK-3 activities |
| Authors: | Chien-Yu Kao;Yi-Chao Hsu;Jen-Wei Liu;Don-Ching Lee;Yu-Fen Chung;Ing-Ming Chiu |
| Contributors: | 聽語學系 |
| Keywords: | FGF1;GSK-3;HDACs;lithium;RFX;VPA |
| Date: | 2013-07-01 |
| Issue Date: | 2015-03-16 15:48:02 (UTC+8) |
| Abstract: | Valproic acid (VPA) is the primary mood-stabilizing drug to exert neuroprotective effects and to treat bipolar disorder in clinic. Fibroblast growth factor 1 (FGF1) has been shown to regulate cell proliferation, cell division, and neurogenesis. Human FGF1 gene 1B promoter (−540 to +31)-driven green fluorescence (F1BGFP) has been shown to recapitulate endogenous FGF1 gene expression and facilitates the isolation of neural stem/progenitor cells (NSPCs) from developing and adult mouse brains. In this study, we provide several lines of evidence to demonstrate the underlying mechanisms of VPA in activating FGF-1B promoter activity: (i) VPA significantly increased the FGF-1B mRNA expression and the percentage of F1BGFP(+) cells; (ii) the increase of F1BGFP expression by VPA involves changes of regulatory factor X (RFX) 1-3 transcriptional complexes and the increase of histone H3 acetylation on the 18-bp cis-element of FGF-1B promoter; (iii) treatments of other histone deacetylases (HDAC) inhibitors, sodium butyrate and trichostatin A, significantly increased the expression levels of FGF-1B, RFX2, and RFX3 transcripts; (iv) treatments of glycogen synthase kinase 3 (GSK-3) inhibitor, lithium, or GSK-3 siRNAs also significantly activated FGF-1B promoter; (v) VPA specifically enhanced neuronal differentiation in F1BGFP(+) embryonic stem cells and NSPCs rather than GFP(−) cells. This study suggested, for the first time, that VPA activates human FGF1 gene promoter through inhibiting HDAC and GSK-3 activities. |
| Relation: | Journal of Neurochemistry, 126(1), 4-18. https://doi.org/10.1111/jnc.12292 |
| Appears in Collections: | [聽力暨語言治療學系] 期刊論文
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