Evidence map›Paper›PMID 34277778›Full record

ArticleAnnals of translational medicine2021

Autophagy attenuates particulate matter 2.5-induced damage in HaCaT cells.

Yu Dai, Yinghui Wang, Sheng Lu, Xuyi Deng, Xinli Niu, Zhi Guo, Rui Qian, Meijuan Zhou, Xuebiao Peng

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

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  5. UPLC-ESI-MS/MS-Based Analysis of Various EdibleFoods (Basel, Switzerland) · 2024
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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

9 authors at 2 institutions in 1 country.

Yu DaiDepartment of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yinghui WangDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Sheng LuThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Xuyi DengDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Xinli NiuDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Zhi GuoDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Rui QianDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Meijuan ZhouDepartment of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Xuebiao PengDepartment of Dermatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKeratinocyte is a key component of the skin barrier and maintains skin homeostasis. As an environmental pathogenic factor, PM2.5 can cause epidermal cell damage, but the mechanism remains to be elucidated. The present study aimed to evaluate the effect caused by PM2.5 in HaCaT cells and investigate the underlying mechanisms.

methodsHaCaT cells were treated with PM2.5 for 12 h or 24 h, either alone or combined with UVB irradiation. A Cell Counting Kit (CCK-8) assay was carried out to detect the effect of PM2.5 on HaCaT cell viability. Flow cytometry, Western Blot, and AO staining were employed to detect the changes of apoptosis and autophagy. The changes of cytotoxicity and apoptosis in HaCaT cells were analyzed by CCK-8 and flow cytometry after pretreatment with autophagy inhibitor 3-MA.

resultsThe results showed that PM2.5 induced cytotoxicity by increasing cell apoptosis and activating autophagy. Apoptosis was determined to be increased significantly after autophagy inhibition. Moreover, solar radiation intensified PM2.5-induced damage in HaCaT cells, which further enhanced the autophagy. However, there was no significant difference in apoptosis after inhibition of autophagy in combined treatment.

conclusionsOur data reveals that PM2.5 induces damage in HaCaT cells, and autophagy plays a protective role to promote cell survival.

Indexed as

apoptosisAutophagycytotoxicityHaCaTPM2.5

Identifiers

PMID34277778
PMCPMC8267295
OpenAlexW3174791495

What OpenQuestion holds

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Registered trials

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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.