Evidence map›Paper›PMID 25347576›Full record

ArticleAmerican journal of respiratory cell and molecular biology2015

Src regulates cigarette smoke-induced ceramide generation via neutral sphingomyelinase 2 in the airway epithelium.

Samuel Chung, Simon Vu, Simone Filosto, Tzipora Goldkorn

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Neutrophil elastase increases airway ceramide levels via upregulation of serine palmitoyltransferase.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  9. Article
  10. Article
  11. Sphingolipids as cell fate regulators in lung development and disease.Apoptosis : an international journal on programmed cell death · 2015
    Review
  12. 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

4 authors at 1 institution in 1 country.

Samuel ChungDepartment of Internal Medicine, Division of Pulmonary and Critical Care, School of Medicine, University of California, Davis, Davis, California.
Simon Vu
Simone Filosto
Tzipora Goldkorn
University of California, Davis · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
THE ROLE OF LACTOSYLCERAMIDE IN RENAL AGING AND DISEASEP20RR017677 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MAO, CUNGUI · 2002 to 2011
$23.4M
MOLECULAR CHARACTERIZATION OF A LUNG SPHINGOMYELINASER01HL066189 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI GOLDKORN, TZIPORA · 2001 to 2013
$2.7M
Proteasome-ErB1 Impaired Interaction in Lung HyperplasiaR01HL071871 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI GOLDKORN, TZIPORA · 2003 to 2006
$1.2M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA138313NCRR NIH HHS P20 RR017677NHLBI NIH HHS HL-66189NHLBI NIH HHS HL-71871NHLBI NIH HHS R01 HL066189NHLBI NIH HHS R01 HL071871
6 · The paper itself

Abstract

We previously demonstrated that the neutral sphingomyelinase (nSMase) 2 is the sole sphingomyelinase activated during cigarette smoke (CS)-induced oxidative stress of human airway epithelial cells, leading to ceramide generation and subsequent apoptosis of affected cells. Since then, we reported that nSMase2 is a phosphoprotein, the degree of enzymatic activity and stability of which are dictated by its degree of phosphorylation. Simultaneously, the non-receptor tyrosine kinase and proto-oncogene Src has increasingly become a target of interest in both smoking-related lung injury, such as chronic obstructive pulmonary disease, and lung cancer. Within this context, we tested and now present Src as a regulator of ceramide generation via modulation of nSMase2 phosphorylation and activity during CS-induced oxidative stress. Specifically, we provide evidence that Src activity is necessary for both CS-induced ceramide accumulation in vivo (129/Sv mice) and in vitro (human airway epithelial cells) and for nSMase2 activity during CS-induced oxidative stress. Moreover, because nSMase2 is exclusively phosphorylated on serines, we show that this occurs through Src-dependent activation of the serine/threonine kinase p38 mitogen-activated protein kinase during oxidative stress. Finally, we provide evidence that Src and p38 mitogen-activated protein kinase activities are critical for regulating nSMase2 phosphorylation. This study provides insights into a molecular target involved in smoking-related lung injury, represented here as nSMase2, and its modulation by the oncogene Src.

Indexed as

AnimalsApoptosisCell Line, TumorCeramidesEnzyme ActivationEpitheliumHumansLung DiseasesMice, 129 StrainOxidative Stressp38 Mitogen-Activated Protein KinasesPhosphorylationProtein Processing, Post-TranslationalProto-Oncogene MasRespiratory MucosaSmokingCeramidesMAS1 protein, humanp38 Mitogen-Activated Protein KinasesProto-Oncogene MasSmpd3 protein, mouseSphingomyelin Phosphodiesterasesrc-Family Kinasesceramideneutral sphingomyelinase 2sphingolipidsSrc

Identifiers

PMID25347576
PMCPMC4491128
OpenAlexW1929776592

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.