Evidence map›Paper›PMID 25349779›Full record

ArticleFEBS open bio2014

Identification of nuclear phosphoproteins as novel tobacco markers in mouse lung tissue following short-term exposure to tobacco smoke.

Kanako Niimori-Kita, Kiyoshi Ogino, Sayaka Mikami, Shinji Kudoh, Daikai Koizumi, Noritaka Kudoh, Fumiko Nakamura, Masahiro Misumi, Tadasuke Shimomura, Koki Hasegawa and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS open bio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  3. Article
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  5. Article
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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

13 authors at 2 institutions in 1 country.

Kanako Niimori-KitaDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Kiyoshi OginoDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Sayaka MikamiAMR Incorporated, 2-13-18, Nakane, Meguro-ku, Tokyo 152-0031, Japan.
Shinji KudohDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Daikai KoizumiDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Noritaka KudohDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Fumiko NakamuraDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Masahiro MisumiDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Tadasuke ShimomuraDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Koki HasegawaDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Fumihiko UsuiAMR Incorporated, 2-13-18, Nakane, Meguro-ku, Tokyo 152-0031, Japan.
Noriyuki NagaharaIsotope Research Center, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.
Takaaki ItoDepartment of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Kumamoto University · JPNippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smoking is a risk factor for lung diseases, including chronic obstructive pulmonary disease and lung cancer. However, the molecular mechanisms mediating the progression of these diseases remain unclear. Therefore, we sought to identify signaling pathways activated by tobacco-smoke exposure, by analyzing nuclear phosphoprotein expression using phosphoproteomic analysis of lung tissue from mice exposed to tobacco smoke. Sixteen mice were exposed to tobacco smoke for 1 or 7 days, and the expression of phosphorylated peptides was analyzed by mass spectrometry. A total of 253 phosphoproteins were identified, including FACT complex subunit SPT16 in the 1-day exposure group, keratin type 1 cytoskeletal 18 (K18), and adipocyte fatty acid-binding protein, in the 7-day exposure group, and peroxiredoxin-1 (OSF3) and spectrin β chain brain 1 (SPTBN1), in both groups. Semi-quantitative analysis of the identified phosphoproteins revealed that 33 proteins were significantly differentially expressed between the control and exposed groups. The identified phosphoproteins were classified according to their biological functions. We found that the identified proteins were related to inflammation, regeneration, repair, proliferation, differentiation, morphogenesis, and response to stress and nicotine. In conclusion, we identified proteins, including OSF3 and SPTBN1, as candidate tobacco smoke-exposure markers; our results provide insights into the mechanisms of tobacco smoke-induced diseases.

Indexed as

60s-RP, 60s ribosomal protein L10EAFABP, adipocyte fatty acid-binding proteinALDH2, aldehyde dehydrogenase, mitochondrialCOPD, chronic obstructive pulmonary disorderCRP1, cysteine and glycine-rich protein 1ERK(1/2), extracellular signal regulated kinase 1/2FACTp140, FACT complex subunit SPT16HIP1, Huntingtin-interacting protein 1IL, interleukinJak2, tyrosine-protein kinase JAK2JNK, c-Jun NH2-terminal kinaseK18, keratin type 1 cytoskeletal 18K8, keratin type 2 cytoskeletal 8LIM, LIM/homeobox proteinMAPK3, mitogen-activated protein kinase 3NF-κB, nuclear factor-kappa BNuclear phosphoproteinOSF3, peroxiredoxin-1p100, serine protease P100Phosphoproteomic analysisPKC-α, protein kinase C-αPRP19, pre-mRNA-processing factor 19pSTAT3-Tyr705, phosphorylated STAT3ROS, reactive oxygen speciesSignaling pathwaysSPTBN1, spectrin β chain brain 1STAT, signal transducer and activator of transcriptionTGF-β, Transforming growth factor-βTIM, mitochondrial import inner membrane translocase subunit Tim9TNFR2, tumor necrosis factor receptor 2TNF, tumor necrosis factorTobacco smoke exposureTRAP1, heat shock protein 75 kDa

Identifiers

PMID25349779
PMCPMC4208089
OpenAlexW2000040356

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.