Evidence map›Paper›PMID 39529607›Full record

ArticleEuropean endodontic journal2024

Possible Involvement of X-Box Binding Protein-1 in the Onset of Pulpitis.

Tomoya Naruse, Katsuhiro Takeda, Kazuma Yoshida, Shinya Sasaki, Tomoki Kumagai, Yohei Takahashi, Reina Kawai, Jun Nakanishi, Hideki Shiba

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European endodontic journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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

2 citing papers in PubMed.

  1. Article
  2. Article
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

9 authors.

Tomoya NaruseDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Katsuhiro TakedaDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kazuma YoshidaDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shinya SasakiDepartment of Periodontal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Tomoki KumagaiDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yohei TakahashiDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Reina KawaiDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Jun NakanishiDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hideki ShibaDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveEndoplasmic reticulum (ER) stress plays important roles not only in stress avoidance, but also in cell differentiation and maturation, cell proliferation, and promotion of bone formation. This study aimed to investigate the involvement of ER stress in the onset of pulpitis.

methodsImmunohistochemical analysis was conducted on human teeth extracted for orthodontic reasons. The effects of tunicamycin (TM), an inducer of ER stress, lipopolysaccharide (LPS), and 4μ8c, an inhibitor of inositol-requiring enzyme 1 (IRE1) on cultured human dental pulp cells (hDPCs) were also examined.

resultsThe expressions of two ER stress markers, X-box binding protein (XBP)-1 and binding immunoglobulin protein (BiP)/78 kDa glucose-regulated protein (GRP78), were found in the human pulp tissues of a decayed tooth that had not developed irreversible acute pulpitis, but not in an impacted tooth without inflammation in pulp tissue. Both TM and LPS increased the mRNA levels of XBP-1, interleukin (IL)-6, and IL-8, whereas TM, but not LPS, enhanced the mRNA expression of BiP/GRP78 in hDPCs. 4μ8c significantly suppressed the increased level of XBP-1 by LPS.

conclusionThis study is the first to demonstrate that XBP-1, in addition to inflammatory cytokines, may participate in the onset of pulpitis through IRE1. These findings provide a more comprehensive understanding of pulpitis pathogenesis through the cooperation of ER stress and inflammatory cytokines.

Indexed as

Dental PulpEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressLipopolysaccharidesPulpitisTranscription FactorsX-Box Binding Protein 1AdolescentCells, CulturedDNA-Binding ProteinsEndoribonucleasesFemaleHeat-Shock ProteinsHumansInterleukin-6Interleukin-8DNA-Binding ProteinsEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN1 protein, humanHeat-Shock ProteinsHSPA5 protein, humanInterleukin-6Interleukin-8LipopolysaccharidesProtein Serine-Threonine KinasesRegulatory Factor X Transcription FactorsTranscription FactorsTunicamycinX-Box Binding Protein 1XBP1 protein, human

Identifiers

PMID39529607
PMCPMC11685515

What Socratic 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 Socratic graph.