Evidence map›Paper›PMID 24919172›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2014

Modeling pulmonary fibrosis by abnormal expression of telomerase/apoptosis/collagen V in experimental usual interstitial pneumonia.

E R Parra, M S Pincelli, W R Teodoro, A P P Velosa, V Martins, M P Rangel, J V Barbas-Filho, V L Capelozzi

Open access · goldAbstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

8 authors at 2 institutions in 1 country.

E R ParraDepartamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
M S PincelliDepartamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
W R TeodoroDisciplina de Reumatologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
A P P VelosaDisciplina de Reumatologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
V MartinsDepartamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
M P RangelDepartamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
J V Barbas-FilhoDepartamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
V L CapelozziDepartamento de Patologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.
Universidade Brasil · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Limitations on tissue proliferation capacity determined by telomerase/apoptosis balance have been implicated in pathogenesis of idiopathic pulmonary fibrosis. In addition, collagen V shows promise as an inductor of apoptosis. We evaluated the quantitative relationship between the telomerase/apoptosis index, collagen V synthesis, and epithelial/fibroblast replication in mice exposed to butylated hydroxytoluene (BHT) at high oxygen concentration. Two groups of mice were analyzed: 20 mice received BHT, and 10 control mice received corn oil. Telomerase expression, apoptosis, collagen I, III, and V fibers, and hydroxyproline were evaluated by immunohistochemistry, in situ detection of apoptosis, electron microscopy, immunofluorescence, and histomorphometry. Electron microscopy confirmed the presence of increased alveolar epithelial cells type 1 (AEC1) in apoptosis. Immunostaining showed increased nuclear expression of telomerase in AEC type 2 (AEC2) between normal and chronic scarring areas of usual interstitial pneumonia (UIP). Control lungs and normal areas from UIP lungs showed weak green birefringence of type I and III collagens in the alveolar wall and type V collagen in the basement membrane of alveolar capillaries. The increase in collagen V was greater than collagens I and III in scarring areas of UIP. A significant direct association was found between collagen V and AEC2 apoptosis. We concluded that telomerase, collagen V fiber density, and apoptosis evaluation in experimental UIP offers the potential to control reepithelization of alveolar septa and fibroblast proliferation. Strategies aimed at preventing high rates of collagen V synthesis, or local responses to high rates of cell apoptosis, may have a significant impact in pulmonary fibrosis.

Indexed as

AnimalsApoptosisButylated HydroxytolueneCell ProliferationCollagen Type ICollagen Type IICollagen Type VDisease Models, AnimalEpithelial CellsFibroblastsFluorescent Antibody TechniqueHydroxyprolineIdiopathic Pulmonary FibrosisImmunohistochemistryIn Situ Nick-End LabelingMaleButylated HydroxytolueneCollagen Type ICollagen Type IICollagen Type VHydroxyprolineTelomerase

Identifiers

PMID24919172
PMCPMC4123836
OpenAlexW2159876959

What OpenQuestion holds

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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.