Evidence map›Paper›PMID 28199407›Full record

ArticlePloS one2017

Keratin14 mRNA expression in human pneumocytes during quiescence, repair and disease.

Marco Confalonieri, Emanuele Buratti, Gabriele Grassi, Rossana Bussani, Marco Chilosi, Rossella Farra, Michela Abrami, Cristiana Stuani, Francesco Salton, Miriam Ficial and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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 4 institutions in 1 country.

Marco ConfalonieriPulmonology Department, University Hospital of Cattinara, Trieste, Italy.
Emanuele BurattiMolecular Pathology, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Gabriele GrassiDepartment of Life Sciences, University of Trieste, Trieste, Italy.
Rossana BussaniInstitute of Pathologic Anatomy, University of Trieste, Trieste, Italy.
Marco ChilosiDepartment of Diagnostic and Public Health, Pathology Unit, University of Verona, Verona, Italy.
Rossella FarraDepartment of Engineering and Architecture, University of Trieste, Trieste, Italy.
Michela AbramiDepartment of Engineering and Architecture, University of Trieste, Trieste, Italy.
Cristiana StuaniMolecular Pathology, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Francesco SaltonPulmonology Department, University Hospital of Cattinara, Trieste, Italy.
Miriam FicialDepartment of Diagnostic and Public Health, Pathology Unit, University of Verona, Verona, Italy.
Paola ConfalonieriPulmonology Department, University Hospital of Cattinara, Trieste, Italy.
Lorenzo ZandonàInstitute of Pathologic Anatomy, University of Trieste, Trieste, Italy.
Maurizio RomanoMolecular Pathology, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
University of Trieste · ITInternational Centre for Genetic Engineering and Biotechnology · ITOspedale di Cattinara · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lung alveoli slowly self-renew pneumocytes, but their facultative regeneration capacity is rapidly efficient after an injury, so fibrosis infrequently occurs. We recently observed Keratin 14 (KRT14) expression during diffuse alveolar damage (DAD), but not in controls. We wonder if KRT14 may be a marker of pneumocyte transition from quiescence to regeneration. Quantitative PCR and Western blot analyses highlighted the presence of KRT14 (mRNA and protein) only in human lung samples with DAD or interstitial lung disease (ILD). In the exponentially growing cell lines A549 and H441, the mRNA and protein levels of KRT14 peaked at day one after cell seeding and decreased at day two, opposite to what observed for the proliferation marker E2F1. The inverse relation of KRT14 versus E2F1 expression holds true also for other proliferative markers, such as cyclin E1 and cyclin D1. Of interest, we also found that E2F1 silencing caused cell cycle arrest and increased KRT14 expression, whilst E2F1 stimulation induced cell cycle progression and decreased KRT14. KRT14 also increased in proliferative pneumocytes (HPAEpiC) just before transdifferentiation. Overall, our results suggest that KRT14 is a viable biomarker of pneumocyte activation, and repair/regeneration. The involvement of KRT14 in regenerative process may suggest a novel pharmaceutical target to accelerate lung repair.

Indexed as

A549 CellsAdolescentAgedAged, 80 and overAlveolar Epithelial CellsCell Cycle CheckpointsCell ProliferationCells, CulturedCell TransdifferentiationCyclin D1Cyclin EE2F1 Transcription FactorFemaleHumansKeratin-14Lung Diseases, InterstitialCCND1 protein, humanCCNE1 protein, humanCyclin D1Cyclin EE2F1 protein, humanE2F1 Transcription FactorKeratin-14Oncogene ProteinsRNA, MessengerRNA, Small Interfering

Identifiers

PMID28199407
PMCPMC5310884
OpenAlexW2588067013

What OpenQuestion holds

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Registered trials

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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.