Evidence map›Paper›PMID 32592329›Full record

ArticleFEBS open bio2020

VNUT/SLC17A9, a vesicular nucleotide transporter, regulates osteoblast differentiation.

Asako Inoue, Kayoko Nakao-Kuroishi, Kaori Kometani-Gunjigake, Masahiro Mizuhara, Tomohiko Shirakawa, Misa Ito-Sago, Kazuma Yasuda, Mitsushiro Nakatomi, Takuma Matsubara, Yukiyo Tada-Shigeyama and 3 more

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 16 citations in OpenAlex.

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  8. The synergism of cytosolic acidosis and reduced NADJournal of biomedical science · 2024
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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

13 authors at 2 institutions in 1 country.

Asako InoueDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Kayoko Nakao-KuroishiDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.ORCID 0000-0001-7704-2821
Kaori Kometani-GunjigakeDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Masahiro MizuharaDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Tomohiko ShirakawaDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Misa Ito-SagoDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Kazuma YasudaDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Mitsushiro NakatomiDivision of Anatomy, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Takuma MatsubaraDivision of Molecular Signaling and Biochemistry, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Yukiyo Tada-ShigeyamaDivision of Dental Anesthesiology, Department of Science of Physical Functions, Kyushu Dental University, Kitakyushu-shi, Japan.
Kazumasa MorikawaDivision of Pediatric and Special Care Dentistry, Department of Developmental Oral Health Science, School of Dentistry, Iwate Medical University, Morioka, Japan.
Shoichiro KokabuDivision of Molecular Signaling and Biochemistry, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Tatsuo KawamotoDivision of Orofacial Functions and Orthodontics, Department of Health Improvement, Kyushu Dental University, Kitakyushu-shi, Japan.
Kyushu Dental University · JPIwate Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoblasts release adenosine triphosphate (ATP) out of the cell following mechanical stress. Although it is well established that extracellular ATP affects bone metabolism via P2 receptors [such as purinergic receptor P2X7 (P2X7R) and purinergic receptor P2Y2 (P2Y2R)], the mechanism of ATP release from osteoblasts remains unknown. Recently, a vesicular nucleotide transporter [VNUT, solute carrier family 17 member 9 (SLC17A9)] that preserves ATP in vesicles has been identified. The purpose of this study was to elucidate the role of VNUT in osteoblast bone metabolism. mRNA and protein expression of VNUT were confirmed in mouse bone and in osteoblasts by quantitative real-time PCR (qPCR) and immunohistochemistry. Next, when compressive force was applied to MC3T3-E1 cells by centrifugation, the expression of Slc17a9, P2x7r, and P2y2r was increased concomitant with an increase in extracellular ATP levels. Furthermore, compressive force decreased the osteoblast differentiation capacity of MC3T3-E1 cells. shRNA knockdown of Slc17a9 in MC3T3-E1 cells reduced levels of extracellular ATP and also led to increased osteoblast differentiation after the application of compressive force as assessed by qPCR analysis of osteoblast markers such as Runx2, Osterix, and alkaline phosphatase (ALP) as well as ALP activity. Consistent with these observations, knockdown of P2x7r or P2y2r by siRNA partially rescued the downregulation of osteoblast differentiation markers, caused by mechanical loading. In conclusion, our results demonstrate that VNUT is expressed in osteoblasts and that VNUT inhibits osteoblast differentiation in response to compressive force by mechanisms related to ATP release and P2X7R and/or P2Y2R activity.

Indexed as

3T3 CellsAnimalsCell DifferentiationCells, CulturedMiceNucleotide Transport ProteinsOsteoblastsNucleotide Transport ProteinsSlc17a9 protein, mouseATPcompressive forceosteoblastosteoblast differentiationP2 receptorVNUT

Identifiers

PMID32592329
PMCPMC7396442
OpenAlexW3037812921

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.