Evidence map›Paper›PMID 25802682›Full record

ArticleOxidative medicine and cellular longevity2015

The loss of cellular junctions in epithelial lung cells induced by cigarette smoke is attenuated by corilagin.

Ximena M Muresan, Franco Cervellati, Claudia Sticozzi, Giuseppe Belmonte, Chung Hin Chui, Ilaria Lampronti, Monica Borgatti, Roberto Gambari, Giuseppe Valacchi

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  7. Review
  8. Inflammasome involvement in CS-induced damage in HaCaT keratinocytes.In vitro cellular & developmental biology. Animal · 2022
    Article
  9. Review
  10. The Role of Connexin 43 in Lung Disease.Life (Basel, Switzerland) · 2020
    Review
  11. Article
  12. Article
  13. Article
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

9 authors at 2 institutions in 2 countries.

Ximena M MuresanDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Franco CervellatiDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Claudia SticozziDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Giuseppe BelmonteDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Chung Hin ChuiClinical Division, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
Ilaria LamprontiBiotechnology Center, University of Ferrara, 44121 Ferrara, Italy.
Monica BorgattiDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Roberto GambariDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Giuseppe ValacchiDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.ORCID 0000-0002-8792-0947
University of Ferrara · ITHong Kong Baptist University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoke (CS) contains over 4700 compounds, many of which can affect cellular redox balance through free radicals production or through the modulation of antioxidant enzymes. The respiratory tract is one of the organs directly exposed to CS and it is known that CS can damage the integrity of lung epithelium by affecting cell junctions and increasing epithelium permeability. In this study, we have used a human lung epithelial cell line, Calu-3, to evaluate the effect of CS on lung epithelial cell junctions levels, with special focus on the expression of two proteins involved in intercellular communication: connexins (Cx) 40 and 43. CS exposure increased Cx40 gene expression but not of Cx43. CS also induced NFκB activation and the formation of 4HNE-Cxs adducts. Since corilagin, a natural polyphenol, is able to inhibit NFκB activation, we have determined whether corilagin could counteract the effect of CS on Cxs expression. Corilagin was able to diminish CS induced Cx40 gene expression, 4HNE-Cx40 adducts formation, and NFκB activation. The results of this study demonstrated that CS induced the loss of cellular junctions in lung epithelium, possibly as a consequence of Cx-4HNE adducts formation, and corilagin seems to be able to abolish these CS induced alterations.

Indexed as

SmokingCell LineConnexin 43ConnexinsElectrophoretic Mobility Shift AssayEpithelial CellsGap Junction alpha-5 ProteinGlucosidesHumansHydrolyzable TanninsIntercellular JunctionsLungMicroscopy, Electron, TransmissionNF-kappa BOxidative StressUp-RegulationConnexin 43ConnexinscorilaginGap Junction alpha-5 ProteinGlucosidesHydrolyzable TanninsNF-kappa B

Identifiers

PMID25802682
PMCPMC4354730
OpenAlexW2040865824

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.