Evidence map›Paper›PMID 26403672›Full record

ArticleJournal of dental research2015

The Role of ORAI1 in the Odontogenic Differentiation of Human Dental Pulp Stem Cells.

S Sohn, Y Park, S Srikanth, A Arai, M Song, B Yu, K-H Shin, M K Kang, C Wang, Y Gwack and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of dental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. GATA Binding Protein 4 Regulates Tooth Root Dentin DevelopmentInternational journal of biological sciences · 2020
    Article
  9. Beclin1 Modulates Bone Homeostasis by Regulating Osteoclast and Chondrocyte Differentiation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. High pH-Sensitive Store-Operated CaFrontiers in physiology · 2018
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

12 authors at 2 institutions in 1 country.

S SohnUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA.
Y ParkUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA.
S SrikanthDepartment of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
A AraiUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA.
M SongUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA.
B YuUCLA School of Dentistry, Los Angeles, CA, USA.
K-H ShinUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA.
M K KangUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA.
C WangUCLA School of Dentistry, Los Angeles, CA, USA UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA.
Y GwackDepartment of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
N-H ParkUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
R H KimUCLA School of Dentistry, Los Angeles, CA, USA Laboratory of Viral Oncology and Aging Research, UCLA School of Dentistry, Los Angeles, CA, USA UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA rkim@dentistry.ucla.edu.
University of California, Los Angeles · USUCLA Jonsson Comprehensive Cancer Center

Funding

Novel regulators of store-operated Ca2+ entry in immune systemsR01AI083432 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GWACK, YOUSANG · 2009 to 2020
$3.8M
Molecular mechanisms of drug-induced ONJ and osteomucosal chronic woundsR01DE023348 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KIM, REUBEN HAN-KYU · 2013 to 2017
$1.9M
Role of oral mucosa in bisphosphonate related osteonecrosis of the jawR03DE021114 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KIM, REUBEN HAN-KYU · 2010 to 2011
$231k
NIAID NIH HHS R01 AI083432NIDCR NIH HHS DE021114NIDCR NIH HHS DE023348NIDCR NIH HHS R01 DE023348NIDCR NIH HHS R03 DE021114
6 · The paper itself

Abstract

Pulp capping, or placing dental materials directly onto the vital pulp tissues of affected teeth, is a dental procedure that aims to regenerate reparative dentin. Several pulp capping materials are clinically being used, and calcium ion (Ca(2+)) released from these materials is known to mediate reparative dentin formation. ORAI1 is an essential pore subunit of store-operated Ca(2+) entry (SOCE), which is a major Ca(2+) influx pathway in most nonexcitable cells. Here, we evaluated the role of ORAI1 in mediating the odontogenic differentiation and mineralization of dental pulp stem cells (DPSCs). During the odontogenic differentiation of DPSCs, the expression of ORAI1 increased in a time-dependent manner. DPSCs knocked down with ORAI1 shRNA (DPSC/ORAI1sh) or overexpressed with dominant negative mutant ORAI1(E106Q) (DPSC/E106Q) exhibited the inhibition of Ca(2+) influx and suppression of odontogenic differentiation and mineralization as demonstrated by alkaline phosphatase (ALP) activity/staining as well as alizarin red S staining when compared with DPSCs of their respective control groups (DPSC/CTLsh and DPSC/CTL). The gene expression for odontogenic differentiation markers such as osteocalcin, bone sialoprotein, and dentin matrix protein 1 (DMP1) was also suppressed. When DPSC/CTL or DPSC/E106Q cells were subcutaneously transplanted into nude mice, DPSC/CTL cells induced mineralized tissue formation with significant increases in ALP and DMP1 staining in vivo, whereas DPSC/E106Q cells did not. Collectively, our data showed that ORAI1 plays critical roles in the odontogenic differentiation and mineralization of DPSCs by regulating Ca(2+) influx and that ORAI1 may be a therapeutic target to enhance reparative dentin formation.

Indexed as

AnimalsCalcium ChannelsCell DifferentiationDental PulpHumansMiceMice, NudeOdontogenesisORAI1 ProteinReal-Time Polymerase Chain ReactionStem CellsStem Cell TransplantationCalcium ChannelsORAI1 ProteinORAI1 protein, humancalciumcalcium release-activated calcium (CRAC) channelsodontogenic mineralizationpulp cappingreparative dentin formationstore-operated calcium entry (SOCE)

Identifiers

PMID26403672
PMCPMC4622325
OpenAlexW2324810052

What OpenQuestion holds

Textmetadata
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.