Funded in part by This work was supported in part by collaborative research grant from Shiseido Co., Ltd. (Kanagawa, Japan)
Elevation of Hyaluronan Synthase by Magnesium Supplementation Mediated through the Activation of GSK3 and CREB in Human Keratinocyte-Derived HaCaT Cells
Marunaka K, Shu S, Kobayashi M, Goto M, Katsuta Y, Yoshino Y, Ikari A
International journal of molecular sciences · 16 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Industry funded
- Government
- Japan Society for the Promotion of Science
- Company
- This work was supported in part by collaborative research grant from Shiseido Co., Ltd. (Kanagawa, Japan)
- Grants
- Japan Society for the Promotion of Science (19H03373)
Based on 2 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2021-12-22 · Int J Mol Sci · vol. 23 · issue 1 · p. 71
- Publisher
- Multidisciplinary Digital Publishing Institute
- Cited
- 27 citations · more than 79% of similar papers · 1.4× the field average
- References
- 31 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Skin and Cellular Biology Research · Wnt/β-catenin signaling in development and cancer · Fibroblast Growth Factor Research
- Keywords
- HaCaT, CREB, Gene knockdown, Hyaluronan synthase, Keratinocyte, Chemistry, Molecular biology, Reporter gene, GSK-3, Glycogen synthase, Gene expression, Biochemistry, Cell biology, Biology, Transcription factor, Kinase, Phosphorylation, Gene, In vitro
- MeSH
- cell line, keratinocytes, skin, humans, magnesium, glycogen synthase kinase 3, hyaluronic acid, rna, messenger, signal transduction, up-regulation, dietary supplements, cyclic amp response element-binding protein, hyaluronan synthases, hacat cells
7 authors
From JP
- Kana MarunakaGifu Pharmaceutical University
- Shokoku ShuGifu Pharmaceutical University
- Mao KobayashiGifu Pharmaceutical University
- Makiko GotoMirai Hospital
- Yuji KatsutaMirai Hospital
- Yuta YoshinoGifu Pharmaceutical University
Abstract
Skin barrier damage is present in the patients with hereditary disorders of the magnesium channel, but the molecular mechanism has not been fully understood. We found that the expressions of hyaluronan synthase (HAS), HAS2 and HAS3 are influenced by MgCl2 concentration in human keratinocyte-derived HaCaT cells. The exposure of cells to a high concentration (5.8 mM) of MgCl2 induced the elevation of HAS2/3 expression, which was inhibited by mRNA knockdown of nonimprinted in Prader-Willi/Angelman syndrome-like domain containing 4 (NIPAL4). Similarly, the content of hyaluronic acid (HA) was changed according to MgCl2 concentration and the expression of NIPAL4. The MgCl2 supplementation increased the reporter activities of HAS2/3, which were inhibited by NIPAL4 knockdown, indicating that the expressions of HAS2/3 are up-regulated at the transcriptional level. The reporter activities and mRNA levels of HAS2/3, and the production of HA were inhibited by CHIR-99021, a glycogen synthase kinase-3 (GSK3) inhibitor, and naphthol AS-E, a cyclic AMP-response element binding protein (CREB) inhibitor. Furthermore, the mutation in putative CREB-binding sites of promoter region in HAS2/3 genes inhibited the MgCl2 supplementation-induced elevation of promoter activity. Our results indicate that the expressions of HAS2/3 are up-regulated by MgCl2 supplementation in HaCaT cells mediated through the activation of GSK3 and CREB. Magnesium may play a pivotal role in maintaining the skin barrier function and magnesium supplementation may be useful to enhance moisturization and wound repair in the skin.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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