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p57<superscript>Kip2</superscript> is an essential regulator of vitamin D receptor-dependent mechanisms.
In: PLoS ONE, Jg. 17 (2023-02-15), Heft 2, S. 1-15
Online
academicJournal
Zugriff:
A cyclin-dependent kinase (CDK) inhibitor, p57Kip2, is an important molecule involved in bone development; p57Kip2-deficient (p57-/-) mice display neonatal lethality resulting from abnormal bone formation and cleft palate. The modulator 1α,25-dihydroxyvitamin D3 (l,25-(OH)2VD3) has shown the potential to suppress the proliferation and induce the differentiation of normal and tumor cells. The current study assessed the role of p57Kip2 in the 1,25-(OH)2VD3-regulated differentiation of osteoblasts because p57Kip2 is associated with the vitamin D receptor (VDR). Additionally, 1,25-(OH)2VD3 treatment increased p57KIP2 expression and induced the colocalization of p57KIP2 with VDR in the osteoblast nucleus. Primary p57-/- osteoblasts exhibited higher proliferation rates with Cdk activation than p57+/+ cells. A lower level of nodule mineralization was observed in p57-/- osteoblasts than in p57+/+ cells. In p57+/+ osteoblasts, 1,25-(OH)2VD3 upregulated the p57Kip2 and opn mRNA expression levels, while the opn expression levels were significantly decreased in p57-/- cells. The osteoclastogenesis assay performed using bone marrow cocultured with 1,25-(OH)2VD3-treated osteoblasts revealed a decreased efficiency of 1,25-(OH)2VD3-stimulated osteoclastogenesis in p57-/- cells. Based on these results, p57Kip2 might function as a mediator of 1,25-(OH)2VD3 signaling, thereby enabling sufficient VDR activation for osteoblast maturation. [ABSTRACT FROM AUTHOR]
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p57<superscript>Kip2</superscript> is an essential regulator of vitamin D receptor-dependent mechanisms.
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Autor/in / Beteiligte Person: | Takahashi, Katsuhiko ; Amano, Hitoshi ; Urano, Tomohiko ; Li, Minqi ; Oki, Meiko ; Aoki, Kazuhiro ; Amizuka, Norio ; Nakayama, Keiichi I. ; Nakayama, Keiko ; Udagawa, Nobuyuki ; Higashi, Nobuaki |
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Zeitschrift: | PLoS ONE, Jg. 17 (2023-02-15), Heft 2, S. 1-15 |
Veröffentlichung: | 2023 |
Medientyp: | academicJournal |
ISSN: | 1932-6203 (print) |
DOI: | 10.1371/journal.pone.0276838 |
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