Evidence map›Paper›PMID 29901090›Full record

ArticleInternational journal of molecular medicine2018

IL‑1β and TNF‑α suppress TGF‑β‑promoted NGF expression in periodontal ligament‑derived fibroblasts through inactivation of TGF‑β‑induced Smad2/3‑ and p38 MAPK‑mediated signals.

Maiko Ohta, Naoyuki Chosa, Seiko Kyakumoto, Seiji Yokota, Naoto Okubo, Akira Nemoto, Masaharu Kamo, Shigeharu Joh, Kenichi Satoh, Akira Ishisaki

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Maiko OhtaDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Shiwa‑gun, Iwate 028‑3694, Japan.
Naoyuki ChosaDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Shiwa‑gun, Iwate 028‑3694, Japan.
Seiko KyakumotoDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Shiwa‑gun, Iwate 028‑3694, Japan.
Seiji YokotaDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Shiwa‑gun, Iwate 028‑3694, Japan.
Naoto OkuboLaboratory of Pathophysiology and Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita‑ku, Sapporo 060‑0812, Japan.
Akira NemotoDivision of Operative Dentistry and Endodontics, Department of Conservative Dentistry, Iwate Medical University, Morioka, Iwate 020‑8505, Japan.
Masaharu KamoDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Shiwa‑gun, Iwate 028‑3694, Japan.
Shigeharu JohDivision of Oral and Dysphasia Rehabilitation, Department of Prosthodontics, Iwate Medical University, Morioka, Iwate 020‑8505, Japan.
Kenichi SatohDivision of Dental Anesthesia, Department of Reconstructive Oral and Maxillofacial Surgery, Iwate Medical University, Morioka, Iwate 020‑8505, Japan.
Akira IshisakiDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Shiwa‑gun, Iwate 028‑3694, Japan.
Iwate Medical University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanosensitive (MS) neurons in the periodontal ligament (PDL) pass information to the trigeminal ganglion when excited by mechanical stimulation of the tooth. During occlusal tooth trauma of PDL tissues, MS neurons are injured, resulting in atrophic neurites and eventual degeneration of MS neurons. Nerve growth factor (NGF), a neurotrophic factor, serves important roles in the regeneration of injured sensory neurons. In the present study, the effect of pro‑inflammatory cytokines, including interleukin 1β (IL‑1β) and tumor necrosis factor α (TNF‑α), on transforming growth factor β1 (TGF‑β1)‑induced NGF expression was evaluated in rat PDL‑derived SCDC2 cells. It was observed that TGF‑β1 promoted NGF expression via Smad2/3 and p38 mitogen‑activated protein kinase (MAPK) activation. IL‑1β and TNF‑α suppressed the TGF‑β1‑induced activation of Smad2/3 and p38 MAPK, resulting in the abrogation of NGF expression. NGF secreted by TGF‑β1‑treated SCDC2 cells promoted neurite extension and the expression of tyrosine hydroxylase, a rate‑limiting enzyme in dopamine synthesis in rat pheochromocytoma PC12 cells. These results suggested that pro‑inflammatory cytokines suppressed the TGF‑β‑mediated expression of NGF in PDL‑derived fibroblasts through the inactivation of TGF‑β‑induced Smad2/3 and p38 MAPK signaling, possibly resulting in the disturbance of the regeneration of injured PDL neurons.

Indexed as

Adenosine TriphosphateAnimalsFibroblastsHumansInterleukin-1betaNerve Growth FactorNeuritesp38 Mitogen-Activated Protein KinasesPC12 CellsPeriodontal LigamentRatsReceptors, Transforming Growth Factor betaRNA, MessengerSignal TransductionSmad ProteinsTransforming Growth Factor betaadenosine 5'-O-(3-thiotriphosphate)Adenosine TriphosphateInterleukin-1betaNerve Growth Factorp38 Mitogen-Activated Protein KinasesReceptors, Transforming Growth Factor betaRNA, MessengerSmad ProteinsTransforming Growth Factor betaTumor Necrosis Factor-alphaTyrosine 3-Monooxygenase

Identifiers

PMID29901090
PMCPMC6089780
OpenAlexW2806023135

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.