Evidence map›Paper›PMID 28652735›Full record

ArticleInternational journal of nanomedicine2017

Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation.

Chengrong Kang, Limin Wei, Bin Song, Liangjiao Chen, Jia Liu, Bin Deng, Xuan Pan, Longquan Shao

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  7. Review
  8. The dual role of autophagy in periprosthetic osteolysis.Frontiers in cell and developmental biology · 2023
    Review
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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

8 authors at 5 institutions in 2 countries.

Chengrong KangDepartment of Stomatology, Nanfang Hospital, Southern Medical University.
Limin WeiDepartment of Stomatology, Nanfang Hospital, Southern Medical University.
Bin SongDepartment of Stomatology, Nanfang Hospital, Southern Medical University.
Liangjiao ChenDepartment of Orthodontics, Key Laboratory of Oral Medicine, Guangzhou Institute of Oral Disease, Stomatology Hospital of Guangzhou Medical University, Guangzhou.
Jia LiuDepartment of Stomatology, Nanfang Hospital, Southern Medical University.
Bin DengDepartment of Stomatology, The General Hospital of People's Liberation Army, Beijing, China.
Xuan PanDepartment of Stomatology, The First Affiliated Hospital of Guangdong Pharmaceutical University.
Longquan ShaoDepartment of Stomatology, Nanfang Hospital, Southern Medical University.
Southern Medical University · CNFirst Affiliated Hospital of Guangdong Pharmaceutical University · CNNanfang Hospital · CNPeople's Liberation Army No. 150 Hospital · CNStomatology Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Porous tantalum (Ta) implants are highly corrosion resistant and biocompatible, and they possess significantly better initial stability than that of conventional titanium (Ti) implants. During loading wear, Ta nanoparticles (Ta-NPs) that were deposited on the surface of a porous Ta implant are inevitably released and come into direct contact with peri-implant osteoblasts. The wear debris may influence cell behavior and implant stabilization. However, the interaction of Ta-NPs with osteoblasts has not been clearly investigated. This study aimed to investigate the effect of Ta-NPs on cell proliferation and their underlying mechanism. The Cell Counting Kit-8 (CCK-8) assay was used to measure the cell viability of MC3T3-E1 mouse osteoblasts and showed that Ta-NP treatment could increase cell viability. Then, confocal microscopy, Western blotting, and transmission electron microscopy were used to confirm the autophagy induced by Ta-NPs, and evidence of autophagy induction was observed as positive LC3 puncta, high-LC3-II expression, and autophagic vesicle ultrastructures. The CCK-8 assay revealed that the cell viability was further increased and decreased by the application of an autophagy inducer and inhibitor, respectively. In addition, pre-treatment with autophagy inhibitor 3-methyladenine (3-MA) inhibited the Ta-NP-induced autophagy. These results indicate that the Ta-NPs can promote cell proliferation, that an autophagy inducer can further strengthen this effect and that an autophagy inhibitor can weaken this effect. In conclusion, autophagy was involved in Ta-NP-induced cell proliferation and had a promoting effect.

Indexed as

AdenineAnimalsAutophagyCell LineCell ProliferationCell SurvivalMiceNanoparticlesOsteoblastsPorosityProstheses and ImplantsTantalum3-methyladenineAdenineTantalumautophagyosteoblastproliferationtantalum nanoparticles

Identifiers

PMID28652735
PMCPMC5473603
OpenAlexW2623490713

What OpenQuestion holds

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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.