Evidence map›Paper›PMID 36791055›Full record

ArticlePloS one2023

p57Kip2 is an essential regulator of vitamin D receptor-dependent mechanisms.

Katsuhiko Takahashi, Hitoshi Amano, Tomohiko Urano, Minqi Li, Meiko Oki, Kazuhiro Aoki, Norio Amizuka, Keiichi I Nakayama, Keiko Nakayama, Nobuyuki Udagawa and 1 more

Abstract read
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In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Katsuhiko TakahashiDepartment of Biochemistry, Hoshi University, Ebara, Shinagawa-ku, Tokyo.
Hitoshi AmanoDepartment of Biochemistry, Hoshi University, Ebara, Shinagawa-ku, Tokyo.ORCID 0000-0001-7370-4832
Tomohiko UranoDepartment of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Minqi LiStomatology Department of Jining Medical University, Jining, and Department of Bone Metabolism, School of Stomatology Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, China.
Meiko OkiDepartment of Basic Oral Health Engineering, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo, Japan.
Kazuhiro AokiDepartment of Basic Oral Health Engineering, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo, Japan.
Norio AmizukaDevelopmental Biology and Hard Tissue, Graduate School of Dental Medicine and Faculty of Dental Medicine, Hokkaido University, Sapporo, Japan.
Keiichi I NakayamaDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi-ku, Fukuoka, Japan.ORCID 0000-0002-7185-1529
Keiko NakayamaDivision of Cell Proliferation, ART, Graduate School of Medicine, Tohoku University, Sendai, Miyagi, Japan.
Nobuyuki UdagawaDepartment of Biochemistry, Matsumoto Dental University, Shiojiri, Japan.
Nobuaki HigashiDepartment of Biochemistry, Hoshi University, Ebara, Shinagawa-ku, Tokyo.ORCID 0000-0001-6803-6147

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Receptors, CalcitriolVitamin DAnimalsCell DifferentiationCell NucleusCyclin-Dependent Kinase Inhibitor p57MiceOsteoblastsCdkn1c protein, mouseCyclin-Dependent Kinase Inhibitor p57Receptors, CalcitriolVdr protein, mouseVitamin D

Identifiers

PMID36791055
PMCPMC9931147

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.