Evidence map›Paper›PMID 33177636›Full record

ArticleScientific reports2020

Effect and underlying mechanisms of airborne particulate matter 2.5 (PM2.5) on cultured human corneal epithelial cells.

Kenji Kashiwagi, Yoko Iizuka

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. PMToxicology and applied pharmacology · 2024
    Article
  9. Greater exposure to PMEnvironmental health : a global access science source · 2024
    Observational
  10. Mechanisms of PMInternational journal of molecular sciences · 2024
    Article
  11. Corneal Vascularization Associated With a Novel PDGFRB Variant.Investigative ophthalmology & visual science · 2023
    Article
  12. Article
  13. Autophagy in the normal and diseased cornea.Experimental eye research · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Kenji KashiwagiDepartment of Ophthalmology, University of Yamanashi, Chuo, Yamanashi, Japan. kenjik@yamanashi.ac.jp.
Yoko IizukaDepartment of Ophthalmology, University of Yamanashi, Chuo, Yamanashi, Japan.
University of Yamanashi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Health problems caused by airborne particulate matter with a diameter less than 2.5 (PM2.5), especially in the respiratory system, have become a worldwide problem, but the influence and mechanisms of PM2.5 on the ocular surface have not been sufficiently elucidated. We investigated in vitro the onset and pathogenesis of corneal damage induced by PM2.5. Two types of PM2.5 samples originating from Beijing (designated #28) and the Gobi Desert (designated #30) were added to the culture medium of immortalized cultured human corneal epithelial cells (HCECs) to examine the effects on survival rates, autophagy, and proinflammatory cytokine production. Both types of PM2.5 significantly reduced the HCEC survival rate in a concentration-dependent manner by triggering autophagy. In particular, compared with #30, #28 induced much more severe damage in HCECs. Physical contact between PM2.5 and HCECs was not a primary contributor to PM2.5-induced HCEC damage. Among the 38 proinflammatory cytokines examined in this study, significant increases in the granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-6 levels and a significant reduction in the interleukin-8 level were detected in culture medium of PM2.5-exposed HCECs. Simultaneous addition of a GM-CSF inhibitor, suramin, alleviated the HCEC impairment induced by PM2.5. In conclusion, PM2.5 induces HCEC death by triggering autophagy. Some cytokines that are released from HCECs, including GM-CSF, may be involved in HCEC damage caused by PM2.5 exposure.

Indexed as

Air PollutantsAutophagyCell LineCell SurvivalChinaCorneaEpithelial CellsGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-2Interleukin-6Interleukin-6 InhibitorsInterleukin-8Particulate MatterSuraminTumor Necrosis Factor-alphaAir PollutantsCSF2 protein, humanCXCL8 protein, humanGranulocyte-Macrophage Colony-Stimulating FactorIL2 protein, humanInterleukin-2Interleukin-6Interleukin-6 InhibitorsInterleukin-8Particulate MatterSuraminTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID33177636
PMCPMC7659009
OpenAlexW3101663251

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.