Evidence map›Paper›PMID 21357385›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2011

Arsenic alters ATP-dependent Ca²+ signaling in human airway epithelial cell wound response.

Cara L Sherwood, R Clark Lantz, Jefferey L Burgess, Scott Boitano

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.0field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Cerium dioxide (CeOEnvironmental research · 2018
    Article
  6. Article
  7. In vivo and in vitro methods for evaluating soil arsenic bioavailability: relevant to human health risk assessment.Journal of toxicology and environmental health. Part B, Critical reviews · 2018
    Review
  8. Article
  9. Plasma membrane wounding and repair in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Arsenic immunotoxicity: a review.Environmental health : a global access science source · 2013
    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

4 authors at 2 institutions in 2 countries.

Cara L SherwoodArizona Respiratory Center, Arizona Health Sciences Center, University of Arizona, Tucson, Arizona 85724-5030, USA.
R Clark Lantz
Jefferey L Burgess
Scott Boitano
West Health · USCollaborative Research Group · AU

Funding

TRANSPORT OF TRACE METALS IN A POLLUTED AQUIFERP42ES004940 · NIEHS · UNIVERSITY OF ARIZONA · PI Jon D Chorover · 1990 to 2026
$68.1M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
PHYSIOLOGYT32HL007249 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson, JOHN P KONHILAS · 1985 to 2026
$12.5M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
PAR2 targeted drug discovery for the treatment of painR01NS073664 · NINDS · UNIVERSITY OF ARIZONA · PI BOITANO, SCOTT, PRICE, THEODORE J. · 2011 to 2015
$1.6M
NHLBI NIH HHS T32 HL007249NHLBI NIH HHS T32-HL007249NIEHS NIH HHS ES 04940NIEHS NIH HHS ES 06694NIEHS NIH HHS P30 ES006694NIEHS NIH HHS P42 ES004940NIEHS NIH HHS T32 ES007091NINDS NIH HHS R01 NS073664
6 · The paper itself

Abstract

Arsenic is a natural metalloid toxicant that is associated with occupational inhalation injury and contaminates drinking water worldwide. Both inhalation of arsenic and consumption of arsenic-tainted water are correlated with malignant and nonmalignant lung diseases. Despite strong links between arsenic and respiratory illness, underlying cell responses to arsenic remain unclear. We hypothesized that arsenic may elicit some of its detrimental effects on the airway through limitation of innate immune function and, specifically, through alteration of paracrine ATP (purinergic) Ca²+ signaling in the airway epithelium. We examined the effects of acute (24 h) exposure with environmentally relevant levels of arsenic (i.e., < 4 μM as Na-arsenite) on wound-induced Ca²+ signaling pathways in human bronchial epithelial cell line (16HBE14o-). We found that arsenic reduces purinergic Ca²+ signaling in a dose-dependent manner and results in a reshaping of the Ca²+ signaling response to localized wounds. We next examined arsenic effects on two purinergic receptor types: the metabotropic P2Y and ionotropic P2X receptors. Arsenic inhibited both P2Y- and P2X-mediated Ca²+ signaling responses to ATP. Both inhaled and ingested arsenic can rapidly reach the airway epithelium where purinergic signaling is essential in innate immune functions (e.g., ciliary beat, salt and water transport, bactericide production, and wound repair). Arsenic-induced compromise of such airway defense mechanisms may be an underlying contributor to chronic lung disease.

Indexed as

Calcium SignalingAdenosine TriphosphateArsenicBronchiEpithelial CellsHumansReverse Transcriptase Polymerase Chain ReactionAdenosine TriphosphateArsenic

Identifiers

PMID21357385
PMCPMC3080191
OpenAlexW2138023657

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.