Evidence map›Paper›PMID 24853558›Full record

ArticleMicrovascular research2014

Cigarette smoke-induced lung endothelial apoptosis and emphysema are associated with impairment of FAK and eIF2α.

Pavlo Sakhatskyy, Gustavo Andres Gabino Miranda, Julie Newton, Chun Geun Lee, Gaurav Choudhary, Alexander Vang, Sharon Rounds, Qing Lu

Open access · greenAbstract read
In one paragraph

Article in Microvascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. CIGARETTE SMOKING INCREASES THE RISK OF ACUTE RESPIRATORY DISTRESS SYNDROME.Transactions of the American Clinical and Climatological Association · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. The Restorative Effect of Red Guava (Veterinary medicine international · 2021
    Article
  13. Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.American journal of respiratory cell and molecular biology · 2020
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  19. Effects of cigarette smoke on pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  20. Pulmonary Endothelial Cell Apoptosis in Emphysema and Acute Lung Injury.Advances in anatomy, embryology, and cell biology · 2018
    Review
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 2 institutions in 1 country.

Pavlo SakhatskyyVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.
Gustavo Andres Gabino MirandaVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.
Julie NewtonVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.
Chun Geun LeePulmonary, Critical Care and Sleep Medicine, School of Medicine, Yale University, New Haven, CT 06520, USA.
Gaurav ChoudharyVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.
Alexander VangVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.
Sharon RoundsVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA.
Qing LuVascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA. Electronic address: Qing_Lu@brown.edu.
Brown University · USYale University · US

Funding

Uncoupling of IL-1 beta and VEGF-A Crosstalk Contributes to Impaired Arteriogenesis Response to Ischemia in Chronic Diabetes MellitusP20GM103652 · NIGMS · OCEAN STATE RESEARCH INSTITUTE, INC. · PI HARRINGTON, ELIZABETH O · 2013 to 2022
$21.3M
Small GTPases and Lung Endothelial ApoptosisR01HL064936 · NHLBI · BROWN UNIVERSITY · PI ROUNDS, SHARON IRENE SMITH · 2000 to 2009
$2.5M
NHLBI NIH HHS HL64936NHLBI NIH HHS R01 HL064936NIGMS NIH HHS P20 GM103652NIGMS NIH HHS P20GM103652
6 · The paper itself

Abstract

Lung endothelial cell (EC) apoptosis has been implicated in the pathogenesis of emphysema. However, the mechanism underlying cigarette smoke (CS)-induced lung EC apoptosis and emphysema is not well defined. We have previously shown that cigarette smoke extract (CSE) decreased focal adhesion kinase (FAK) activity via oxidative stress in cultured lung EC. In this study, we compared FAK activation in the lungs of highly susceptible AKR mice and mildly susceptible C57BL/6 mice after exposure to CS for three weeks. We found that three weeks of CS exposure caused mild emphysema and increased lung EC apoptosis in AKR mice (room air: 12.8±5.6%; CS: 30.7±3.7%), but not in C57BL/6 mice (room air: 0±0%; CS: 3.5±1.7%). Correlated with increased lung EC apoptosis and early onset of emphysema, FAK activity was reduced in the lungs of AKR mice, but not of C57BL/6 mice. Additionally, inhibition of FAK caused lung EC apoptosis, whereas over-expression of FAK prevented CSE-induced lung EC apoptosis. These results suggest that FAK inhibition may contribute to CS-induced lung EC apoptosis and emphysema. Unfolded protein response (UPR) and autophagy have been shown to be activated by CS exposure in lung epithelial cells. In this study, we noted that CSE activated UPR and autophagy in cultured lung EC, as indicated by enhanced eIF2α phosphorylation and elevated levels of GRP78 and LC3B-II. However, eIF2α phosphorylation was significantly reduced by three-weeks of CS exposure in the lungs of AKR mice, but not of C57BL/6 mice. Markers for autophagy activation were not significantly altered in the lungs of either AKR or C57BL/6 mice. These results suggest that CS-induced impairment of eIF2α signaling may increase the susceptibility to lung EC apoptosis and emphysema. Taken together, our data suggest that inhibition of eIF2α and FAK signaling may play an important role in CS-induced lung EC apoptosis and emphysema.

Indexed as

ApoptosisAnimalsAutophagyCattleCells, CulturedEmphysemaEndoplasmic Reticulum Chaperone BiPEndothelial CellsEukaryotic Initiation Factor-2Focal Adhesion Kinase 1Gene Expression RegulationHeat-Shock ProteinsLungMaleMiceMice, Inbred AKREndoplasmic Reticulum Chaperone BiPEukaryotic Initiation Factor-2Focal Adhesion Kinase 1Heat-Shock ProteinsHspa5 protein, mousePtk2 protein, mouseSmokeAKR miceApoptosisAutophagyCigarette smokeeIF2alphaEmphysemaEndothelial cellFocal adhesion kinaseLungUnfolded protein response

Identifiers

PMID24853558
PMCPMC4185927
OpenAlexW1973774591

What OpenQuestion holds

Textmetadata
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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.