Evidence map›Paper›PMID 38419076›Full record

ArticleParticle and fibre toxicology2024

Zinc oxide nanoparticles exacerbate skin epithelial cell damage by upregulating pro-inflammatory cytokines and exosome secretion in M1 macrophages following UVB irradiation-induced skin injury.

Bour-Jr Wang, Yu-Ying Chen, Hui-Hsuan Chang, Rong-Jane Chen, Ying-Jan Wang, Yu-Hsuan Lee

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

6 authors at 3 institutions in 1 country.

Bour-Jr Wang *Department of Cosmetic Science and Institute of Cosmetic Science, Chia Nan University of Pharmacy and Science, Tainan, 71710, Taiwan.
Yu-Ying Chen *Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan, 70428, Taiwan.
Hui-Hsuan ChangDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan, 70428, Taiwan.
Rong-Jane ChenDepartment of Food Safety/Hygiene and Risk Management, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan, 70428, Taiwan.
Ying-Jan WangDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan, 70428, Taiwan. yjwang@mail.ncku.edu.tw.
Yu-Hsuan LeeDepartment of Cosmeceutics, China Medical University, Taichung, 406040, Taiwan. yhlee@mail.cmu.edu.tw.
National Cheng Kung University · TWChia Nan University of Pharmacy and Science · TWChina Medical University · TW

Funding

China Medical University, Taichung, Taiwan CMU112-S-50National Science and Technology Council MOST 109-2314-B-006-051-MY3National Science and Technology Council MOST 110-2314-B-039-018Toxic and Chemical Substance Bureau, Taiwan 110A012
6 · The paper itself

Abstract

backgroundZinc oxide nanoparticles (ZnONPs) are common materials used in skin-related cosmetics and sunscreen products due to their whitening and strong UV light absorption properties. Although the protective effects of ZnONPs against UV light in intact skin have been well demonstrated, the effects of using ZnONPs on damaged or sunburned skin are still unclear. In this study, we aimed to reveal the detailed underlying mechanisms related to keratinocytes and macrophages exposed to UVB and ZnONPs.

resultsWe demonstrated that ZnONPs exacerbated mouse skin damage after UVB exposure, followed by increased transepidermal water loss (TEWL) levels, cell death and epithelial thickness. In addition, ZnONPs could penetrate through the damaged epithelium, gain access to the dermis cells, and lead to severe inflammation by activation of M1 macrophage. Mechanistic studies indicated that co-exposure of keratinocytes to UVB and ZnONPs lysosomal impairment and autophagy dysfunction, which increased cell exosome release. However, these exosomes could be taken up by macrophages, which accelerated M1 macrophage polarization. Furthermore, ZnONPs also induced a lasting inflammatory response in M1 macrophages and affected epithelial cell repair by regulating the autophagy-mediated NLRP3 inflammasome and macrophage exosome secretion.

conclusionsOur findings propose a new concept for ZnONP-induced skin toxicity mechanisms and the safety issue of ZnONPs application on vulnerable skin. The process involved an interplay of lysosomal impairment, autophagy-mediated NLRP3 inflammasome and macrophage exosome secretion. The current finding is valuable for evaluating the effects of ZnONPs for cosmetics applications.

Indexed as

ExosomesNanoparticlesZinc OxideAnimalsCytokinesEpithelial CellsInflammasomesMiceNLR Family, Pyrin Domain-Containing 3 ProteinUltraviolet RaysCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinZinc OxideAutophagy dysfunctionExosomeLysosomal impairmentMacrophage polarizationTransepidermal water lossZinc oxide nanoparticle

Identifiers

PMID38419076
PMCPMC10900617
OpenAlexW4392239079

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.