Evidence map›Paper›PMID 37533959›Full record

ArticleTobacco induced diseases2023

Cigarette smoking exposure disrupts the regenerative potential of dental pulp stem cells.

Leyla Tahrani Hardin, David Vang, Der Thor, Xiaoyuan Han, Fatima Mashkoor, Tamer Alpagot, David M Ojcius, Nan Xiao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Tobacco induced diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

8 authors at 1 institution in 2 countries.

Leyla Tahrani HardinDepartment of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
David VangDepartment of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
Der ThorDepartment of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
Xiaoyuan HanDepartment of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
Fatima MashkoorDepartment of Oral and Maxillofacial Surgery, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
Tamer AlpagotDepartment of Periodontics, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
David M OjciusDepartment of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
Nan XiaoDepartment of Biomedical Sciences, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, United States.
University of the Pacific · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSmoking is known to alter the regenerative and immunomodulatory properties of many types of mesenchymal stem cells (MSCs). This study investigates the impact of cigarette smoke exposure on the regenerative potential of dental pulp stem cells (DPSCs).

methodsDPSCs were treated with various doses of cigarette smoke condensate (CSC) or nicotine. Cell proliferation and survival were evaluated by a water-soluble tetrazolium salt (WST-1) and a survival assay. DPSC migration, cytokine expression, mutagenesis, and the signaling pathway were also measured during CSC and nicotine treatment.

resultsLow concentrations of CSC and nicotine did not impair cell proliferation, but higher concentrations reduced cell proliferation. CSC and nicotine could impede DPSC survival and migration in a dose-dependent manner. In addition, the cytokine secretion expression profile was altered with CSC or nicotine treatments. In particular, secretion of IL-6, TNF-α, and IL-10 significantly increased, while TGF-β1 levels showed different patterns after exposure to CSC or nicotine, as shown by ELISA and quantitative PCR. Nicotine treatment increased AKT (also known as protein kinase B) and extracellular signal-regulated kinase (ERK) phosphorylation. Finally, CSC induced higher levels of mutagenicity than nicotine, as shown by the Ames test.

conclusionsThese findings suggest that cigarette smoke exposure alters the regenerative abilities of DPSCs in various ways. Future studies are warranted to further characterize the underlying molecular mechanisms of smoking-mediated damage to DPSCs, which will guide the personalized stem cell treatment plan for smoking patients.

Indexed as

DPSCsinflammationnicotineregenerationsmoking

Identifiers

PMID37533959
PMCPMC10392041
OpenAlexW4385445019

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.