Evidence map›Paper›PMID 35087028›Full record

ArticleInternational journal of oral science2022

The role of complement C5a receptor in DPSC odontoblastic differentiation and in vivo reparative dentin formation.

Muhammad Irfan, Ji-Hyun Kim, Hassan Marzban, David A Reed, Anne George, Lyndon F Cooper, Seung Chung

Open access · goldAbstract read
In one paragraph

Article in International journal of oral science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 28 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

7 authors at 2 institutions in 2 countries.

Muhammad IrfanDepartment of Oral Biology, University of Illinois at Chicago, Chicago, USA.
Ji-Hyun KimDepartment of Oral Biology, University of Illinois at Chicago, Chicago, USA.
Hassan MarzbanDepartment of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada.
David A ReedDepartment of Oral Biology, University of Illinois at Chicago, Chicago, USA.ORCID http://orcid.org/0000-0001-9121-0932
Anne GeorgeDepartment of Oral Biology, University of Illinois at Chicago, Chicago, USA.
Lyndon F CooperDepartment of Oral Biology, University of Illinois at Chicago, Chicago, USA.
Seung ChungDepartment of Oral Biology, University of Illinois at Chicago, Chicago, USA. chungsh@uic.edu.ORCID http://orcid.org/0000-0003-1449-8762
University of Illinois Chicago · USUniversity of Manitoba · CA

Funding

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 DE029816NIDCR NIH HHS R03 DE028637NIDCR NIH HHS R56 DE029816
6 · The paper itself

Abstract

Therapeutic dentin regeneration remains difficult to achieve, and a majority of the attention has been given to anabolic strategies to promote dentinogenesis directly, whereas, the available literature is insufficient to understand the role of inflammation and inflammatory complement system on dentinogenesis. The aim of this study is to determine the role of complement C5a receptor (C5aR) in regulating dental pulp stem cells (DPSCs) differentiation and in vivo dentin regeneration. Human DPSCs were subjected to odontogenic differentiation in osteogenic media treated with the C5aR agonist and C5aR antagonist. In vivo dentin formation was evaluated using the dentin injury/pulp-capping model of the C5a-deficient and wild-type mice. In vitro results demonstrate that C5aR inhibition caused a substantial reduction in odontogenic DPSCs differentiation markers such as DMP-1 and DSPP, while the C5aR activation increased these key odontogenic genes compared to control. A reparative dentin formation using the C5a-deficient mice shows that dentin regeneration is significantly reduced in the C5a-deficient mice. These data suggest a positive role of C5aR in the odontogenic DPSCs differentiation and tertiary/reparative dentin formation. This study addresses a novel regulatory pathway and a therapeutic approach for improving the efficiency of dentin regeneration in affected teeth.

Indexed as

Dental PulpStem CellsAnimalsCell DifferentiationCells, CulturedComplement C5aDentinMiceReceptor, Anaphylatoxin C5aC5ar1 protein, mouseComplement C5aReceptor, Anaphylatoxin C5a

Identifiers

PMID35087028
PMCPMC8795457
OpenAlexW4210599971

What OpenQuestion holds

Textmetadata
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.