Evidence map›Paper›PMID 16051704›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide.

Hong Pyo Kim, Xue Wang, Atsunori Nakao, Sung Il Kim, Noriko Murase, Mary E Choi, Stefan W Ryter, Augustine M K Choi

Erratum issuedOpen access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Therapeutic Aspects of Carbon Monoxide in Cardiovascular Disease.International journal of molecular sciences · 2018
    Review
  7. Article
  8. Carbon monoxide in lung cell physiology and disease.American journal of physiology. Cell physiology · 2018
    Review
  9. Review
  10. Review
  11. Targeting heme oxygenase-1 and carbon monoxide for therapeutic modulation of inflammation.Translational research : the journal of laboratory and clinical medicine · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. p38β, A novel regulatory target of Pokemon in hepatic cells.International journal of molecular sciences · 2013
    Article
  17. Article
  18. Carbon monoxide: present and future indications for a medical gas.The Korean journal of internal medicine · 2013
    Review
  19. Therapeutic applications of carbon monoxide.Oxidative medicine and cellular longevity · 2013
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Hong Pyo KimDivision of Pulmonary, Allergy, and Critical Care Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Xue Wang
Atsunori Nakao
Sung Il Kim
Noriko Murase
Mary E Choi
Stefan W Ryter
Augustine M K Choi
University of Pittsburgh · USHouston Methodist · US

Funding

The Role of HEME Oxygenase in Hyperoxic Lung InjuryR01HL055330 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1998 to 2021
$6.6M
HEME OXYGENASE 1--LUNG VASCULAR CELL HYPOXIC RESPONSER01HL060234 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1999 to 2017
$5.8M
HEME OXYGENASE-1 AND SEPSIS USING TRANSGENIC MICER01AI042365 · NIAID · YALE UNIVERSITY · PI CHOI, AUGUSTINE M · 1998 to 2002
$691k
NHLBI NIH HHS R01 HL055330NHLBI NIH HHS R01 HL060234NHLBI NIH HHS R01-HL55330NHLBI NIH HHS R01-HL60234NIAID NIH HHS R01-AI42365
6 · The paper itself

Abstract

During vascular injury, the proliferation and migration of smooth muscle cells leads to characteristic neointima formation, which can be exacerbated by genetic depletion of caveolin-1 or heme oxygenase 1 (HO-1), and inhibited by carbon monoxide (CO), a by-product of heme oxygenase 1 activity. CO inhibited smooth muscle cell proliferation by activating p38 mitogen-activated protein kinase (MAPK) and p21(Waf1/Cip1). Exposure to CO increased caveolin-1 expression in neointimal lesions of injured aorta and in vitro by activating guanylyl cyclase and p38 MAPK. p38beta-/- fibroblasts did not induce caveolin-1 in response to CO, and exhibited a diminished basal caveolin-1 expression, which was restored by p38beta gene transfer. p38beta MAPK down-regulated extracellular signal-regulated protein kinase 1/2 (ERK-1/2), which can repress caveolin-1 transcription. Genetic depletion of caveolin-1 abolished the antiproliferative effect of CO. Thus, we demonstrate that CO, by activating p38beta MAPK, up-regulates caveolin-1, which acts as a tumor suppressor protein that mediates the growth inhibitory properties of this gas.

Indexed as

Gene Expression RegulationAnimalsAortaBlotting, WesternCarbon MonoxideCell MovementCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Enzyme ActivationFibroblastsGene Transfer TechniquesGuanylate CyclaseHeme Oxygenase (Decyclizing)ImmunohistochemistryImmunoprecipitationCarbon MonoxideCdkn1a protein, ratCyclin-Dependent Kinase Inhibitor p21Guanylate CyclaseHeme Oxygenase (Decyclizing)Mitogen-Activated Protein Kinase 11RNA, Small InterferingThymidineTritium

Identifiers

PMID16051704
PMCPMC1183544
OpenAlexW2040755930

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.