Evidence map›Paper›PMID 17936186›Full record

ArticleFree radical biology & medicine2007

N-acetylcysteine protects dental pulp stromal cells from HEMA-induced apoptosis by inducing differentiation of the cells.

Avina Paranjpe, Nicholas A Cacalano, Wyatt R Hume, Anahid Jewett

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 88 citations in OpenAlex.

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  18. Cellular antioxidant levels influence muscle stem cell therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2010
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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

4 authors at 1 institution in 1 country.

Avina ParanjpeThe Jane and Jerry Weintraub Center for Reconstructive Biotechnology, Dental Research Institute, Division of Oral Biology and Medicine, UCLA School of Dentistry and Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Nicholas A Cacalano
Wyatt R Hume
Anahid Jewett
University of California, Los Angeles · US

Funding

CHEMICAL RELEASE &IMMUNE SENSITIZATION BY DENTAL RESINSR01DE010331 · NIDCR · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI JEWETT, ANAHID · 1993 to 2002
$654k
NIDCR NIH HHS R01 DE010331PHS HHS R01-10331
6 · The paper itself

Abstract

Resin-based materials are now widely used in dental restorations. Although the use of these materials is aesthetically appealing to patients, it carries the risk of local and systemic adverse effects. The potential risks are direct damage to the cells and induction of immune-based hypersensitivity reactions. Dental pulp stromal cells (DPSCs) and oral keratinocytes are the major cell types which may come in contact with dental resins such as 2-hydroxyethyl methacrylate (HEMA) after dental restorations. Here we show that N-acetylcysteine (NAC) inhibits HEMA-induced apoptotic cell death and restores the function of DPSCs and oral epithelial cells. NAC inhibits HEMA-mediated toxicity through induction of differentiation in DPSCs, because the genes for dentin sialoprotein, osteopontin (OPN), osteocalcin, and alkaline phosphatase, which are induced during differentiation, are also induced by NAC. Unlike NAC, vitamins E and C, which are known antioxidant compounds, failed to prevent either HEMA-mediated cell death or the decrease in VEGF secretion by human DPSCs. More importantly, when added either alone or in combination with HEMA, vitamin E and vitamin C did not increase the gene expression for OPN, and in addition vitamin E inhibited the protective effect of NAC on DPSCs. NAC inhibited the HEMA-mediated decrease in NF-kappaB activity, thus providing a survival mechanism for the cells. Overall, the studies reported in this paper indicate that undifferentiated DPSCs have exquisite sensitivity to HEMA-induced cell death, and their differentiation in response to NAC resulted in an increased NF-kappaB activity, which might have provided the basis for their increased protection from HEMA-mediated functional loss and cell death.

Indexed as

AcetylcysteineAlkaline PhosphataseApoptosisAscorbic AcidCell DifferentiationCell ProliferationCytoprotectionDental PulpFree Radical ScavengersGene ExpressionHumansMethacrylatesNF-kappa BStromal CellsVascular Endothelial Growth Factor AVitamin EAcetylcysteineAlkaline PhosphataseAscorbic AcidFree Radical Scavengershydroxyethyl methacrylateMethacrylatesNF-kappa BVascular Endothelial Growth Factor AVitamin E

Identifiers

PMID17936186
PMCPMC2134970
OpenAlexW2042101534

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.