Evidence map›Paper›PMID 27644844›Full record

ArticleScientific reports2016

Protein oxidation and degradation caused by particulate matter.

Ching-Huang Lai, Chun-Nin Lee, Kuan-Jen Bai, You-Lan Yang, Kai-Jen Chuang, Sheng-Ming Wu, Hsiao-Chi Chuang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 41 citations in OpenAlex.

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  10. Alterations by Air Pollution in Inflammation and Metals in Pleural Effusion of Pneumonia Patients.International journal of environmental research and public health · 2019
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  11. 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

7 authors at 3 institutions in 1 country.

Ching-Huang LaiSchool of Public Health, National Defense Medical Center, Taipei, Taiwan.
Chun-Nin LeeSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Kuan-Jen BaiSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
You-Lan YangSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Kai-Jen ChuangDepartment of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Sheng-Ming WuDivision of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Hsiao-Chi ChuangSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Taipei Medical University · TWNational Defense Medical Center · TWTaipei Medical University-Shuang Ho Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Particulate matter (PM) modulates the expression of autophagy; however, the role of selective autophagy by PM remains unclear. The objective of this study was to determine the underlying mechanisms in protein oxidation and degradation caused by PM. Human epithelial A549 cells were exposed to diesel exhaust particles (DEPs), urban dust (UD), and carbon black (CB; control particles). Cell survival and proliferation were significantly reduced by DEPs and UD in A549 cells. First, benzo(a)pyrene diolepoxide (BPDE) protein adduct was caused by DEPs at 150 μg/ml. Methionine oxidation (MetO) of human albumin proteins was induced by DEPs, UD, and CB; however, the protein repair mechanism that converts MetO back to methionine by methionine sulfoxide reductases A (MSRA) and B3 (MSRB3) was activated by DEPs and inhibited by UD, suggesting that oxidized protein was accumulating in cells. As to the degradation of oxidized proteins, proteasome and autophagy activation was induced by CB with ubiquitin accumulation, whereas proteasome and autophagy activation was induced by DEPs without ubiquitin accumulation. The results suggest that CB-induced protein degradation may be via an ubiquitin-dependent autophagy pathway, whereas DEP-induced protein degradation may be via an ubiquitin-independent autophagy pathway. A distinct proteotoxic effect may depend on the physicochemistry of PM.

Indexed as

A549 CellsAlbuminsHumansMethionine Sulfoxide ReductasesOxidation-ReductionParticulate MatterProteolysisVehicle EmissionsAlbuminsmethionine sulfoxide reductaseMethionine Sulfoxide ReductasesMSRB3 protein, humanParticulate MatterVehicle Emissions

Identifiers

PMID27644844
PMCPMC5028717
OpenAlexW2523026210

What OpenQuestion holds

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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.