Evidence map›Paper›PMID 37247252›Full record

ArticleConnective tissue research2023

LPS-induced inflammation potentiates dental pulp stem cell odontogenic differentiation through C5aR and p38.

Ji-Hyun Kim, Muhammad Irfan, Md Akil Hossain, Susie Shin, Anne George, Seung Chung

Open access · greenAbstract read
In one paragraph

Article in Connective tissue research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Dual effects of 1α,25-dihydroxyvitamin DJournal of dental sciences · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. CaFrontiers in cell and developmental biology · 2025
    Article
  11. Dental Stem Cells and Lipopolysaccharides: A Concise Review.International journal of molecular sciences · 2024
    Review
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Ji-Hyun KimDepartment of Oral Biology, University of Illinois Chicago, Chicago, IL, USA.
Muhammad IrfanDepartment of Oral Biology, University of Illinois Chicago, Chicago, IL, USA.
Md Akil HossainDepartment of Oral Biology, University of Illinois Chicago, Chicago, IL, USA.
Susie ShinDepartment of Oral Biology, University of Illinois Chicago, Chicago, IL, USA.
Anne GeorgeDepartment of Oral Biology, University of Illinois Chicago, Chicago, IL, USA.
Seung ChungDepartment of Oral Biology, University of Illinois Chicago, Chicago, IL, USA.
University of Illinois Chicago · US

Funding

Role of DMP1 Mediated Paracrine Signaling in VasculogenesisR01DE031737 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Anne George · 2022 to 2026
$2.5M
The Role of DPP in Dental Pulp Stem Cells and its Potential in Tissue RegenerationR01DE028531 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GEORGE, ANNE · 2019 to 2023
$1.9M
Role of complement receptor C5L2 in reparative dentinogenesisR01DE029816 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHUNG, SEUNG · 2022 to 2025
$1.9M
Role of complement receptor C5L2 in reparative dentinogenesisR56DE029816 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHUNG, SEUNG · 2020 to 2020
$380k
Pulp fibroblast-mediated inferior alveolar nerve regenerationR03DE028637 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHUNG, SEUNG · 2020 to 2021
$320k
NIDCR NIH HHS R01 DE028531NIDCR NIH HHS R01 DE029816NIDCR NIH HHS R01 DE031737NIDCR NIH HHS R03 DE028637NIDCR NIH HHS R56 DE029816
6 · The paper itself

Abstract

aimInflammation is a complex host response to harmful infection or injury, and it seems to play a crucial role in tissue regeneration both positively and negatively. We have previously demonstrated that the activation of the complement C5a pathway affects dentin-pulp regeneration. However, limited information is available to understand the role of the complement C5a system related to inflammation-mediated dentinogenesis. The aim of this study was to determine the role of complement C5a receptor (C5aR) in regulating lipopolysaccharide (LPS)-induced odontogenic differentiation of dental pulp stem cells (DPSCs). MATERIAL AND

methodsHuman DPSCs were subjected to LPS-stimulated odontogenic differentiation in dentinogenic media treated with the C5aR agonist and antagonist. A putative downstream pathway of the C5aR was examined using a p38 mitogen-activated protein kinase (p38) inhibitor (SB203580).

resultsOur data demonstrated that inflammation induced by the LPS treatment potentiated DPSC odontogenic differentiation and that this is C5aR dependent. C5aR signaling controlled the LPS-stimulated dentinogenesis by regulating the expression of odontogenic lineage markers like dentin sialophosphoprotein (DSPP) and dentin matrix protein 1 (DMP-1). Moreover, the LPS treatment increased the total p38, and the active form of p38 expression, and treatment with SB203580 abolished the LPS-induced DSPP and DMP-1 increase.

conclusionsThese data suggest a significant role of C5aR and its putative downstream molecule p38 in the LPS-induced odontogenic DPSCs differentiation. This study highlights the regulatory pathway of complement C5aR/p38 and a possible therapeutic approach for improving the efficiency of dentin regeneration during inflammation.

Indexed as

Dental PulpLipopolysaccharidesCell DifferentiationCell ProliferationCells, CulturedComplement C5aHumansInflammationMitogen-Activated Protein Kinase 14Receptor, Anaphylatoxin C5aRegenerationStem CellsC5AR1 protein, humanComplement C5aLipopolysaccharidesMitogen-Activated Protein Kinase 14Receptor, Anaphylatoxin C5aC5a ReceptorcariesdentinogenesisDMP-1DSPP

Identifiers

PMID37247252
PMCPMC10524681
OpenAlexW4378650155

What OpenQuestion holds

Textmetadata
LicenceTDM
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.