Evidence map›Paper›PMID 22592920›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Hydrogen sulfide attenuates particulate matter-induced human lung endothelial barrier disruption via combined reactive oxygen species scavenging and Akt activation.

Ting Wang, Lichun Wang, Syed R Zaidi, Saad Sammani, Jessica Siegler, Liliana Moreno-Vinasco, Biji Mathew, Viswanathan Natarajan, Joe G N Garcia

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Targeted HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021
    Article
  6. Article
  7. Endothelium as a Source and Target of HAntioxidants (Basel, Switzerland) · 2021
    Review
  8. HIntensive care medicine experimental · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Vascular biology of hydrogen sulfide.American journal of physiology. Cell physiology · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

Ting WangDepartment of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
Lichun Wang
Syed R Zaidi
Saad Sammani
Jessica Siegler
Liliana Moreno-Vinasco
Biji Mathew
Viswanathan Natarajan
Joe G N Garcia
University of Illinois Chicago · US

Funding

Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GARCIA, JOE G. N. · 1998 to 2012
$27.8M
NHLBI NIH HHS HL058064NHLBI NIH HHS P01 HL058064
6 · The paper itself

Abstract

Exposure to particulate air pollution is associated with increased cardiopulmonary morbidity and mortality, although the pathogenic mechanisms are poorly understood. We previously demonstrated that particulate matter (PM) exposure triggers massive oxidative stress in vascular endothelial cells (ECs), resulting in the loss of EC integrity and lung vascular hyperpermeability. We investigated the protective role of hydrogen sulfide (H(2)S), an endogenous gaseous molecule present in the circulation, on PM-induced human lung EC barrier disruption and pulmonary inflammation. Alterations in EC monolayer permeability, as reflected by transendothelial electrical resistance (TER), the generation of reactive oxygen species (ROS), and murine pulmonary inflammatory responses, were studied after exposures to PM and NaSH, an H(2)S donor. Similar to N-acetyl cysteine (5 mM), NaSH (10 μM) significantly scavenged PM-induced EC ROS and inhibited the oxidative activation of p38 mitogen-activated protein kinase. Concurrent with these events, NaSH (10 μM) activated Akt, which helps maintain endothelial integrity. Both of these pathways contribute to the protective effect of H(2)S against PM-induced endothelial barrier dysfunction. Furthermore, NaSH (20 mg/kg) reduced vascular protein leakage, leukocyte infiltration, and proinflammatory cytokine release in bronchoalveolar lavage fluids in a murine model of PM-induced lung inflammation. These data suggest a potentially protective role for H(2)S in PM-induced inflammatory lung injury and vascular hyperpermeability.

Indexed as

AnimalsCapillary PermeabilityCells, CulturedElectric ImpedanceEndothelial CellsEnzyme ActivationFree Radical ScavengersHumansHydrogen SulfideLungMaleMAP Kinase Signaling SystemMiceMicrovesselsp38 Mitogen-Activated Protein KinasesParticulate MatterFree Radical ScavengersHydrogen Sulfidep38 Mitogen-Activated Protein KinasesParticulate MatterProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID22592920
PMCPMC3488621
OpenAlexW2026695480

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.