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Financiado en parte por 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 citas

Etiquetas de revisión

Financiado por la industriaSolo mecanismos

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Cómo se estudió

Diseño
Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
Estudiado en
Células o muestras de laboratorio
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiado por la industria
Gobierno
Japan Society for the Promotion of Science
Empresa
This work was supported in part by collaborative research grant from Shiseido Co., Ltd. (Kanagawa, Japan)
Subvenciones
Japan Society for the Promotion of Science (19H03373)

Según 2 financiadores declarados y la declaración de financiación del texto completo.

Publicación

Publicado
2021-12-22 · Int J Mol Sci · vol. 23 · número 1 · pág. 71
Editorial
Multidisciplinary Digital Publishing Institute
Citado
27 citas · más que el 79% de estudios similares · 1.4× el promedio de su campo
Referencias
31 trabajos
Acceso
Acceso abierto (revista) · CC-BY
Áreas de investigación
Skin and Cellular Biology Research · Wnt/β-catenin signaling in development and cancer · Fibroblast Growth Factor Research
Palabras clave
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 autores

  • Kana Marunaka🇯🇵Gifu Pharmaceutical University
  • Shokoku Shu🇯🇵Gifu Pharmaceutical University
  • Mao Kobayashi🇯🇵Gifu Pharmaceutical University
  • Makiko Goto🇯🇵Mirai Hospital
  • Yuji Katsuta🇯🇵Mirai Hospital
  • Yuta Yoshino🇯🇵Gifu Pharmaceutical University
  • Akira Ikari🇯🇵 · autor de correspondenciaGifu Pharmaceutical University

Resumen

El texto original del estudio, en el idioma en que se publicó.

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.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).

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