Evidence map›Paper›PMID 38002017›Full record

ArticleBiomedicines2023

Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes.

Áron Dernovics, György Seprényi, Zsolt Rázga, Ferhan Ayaydin, Zoltán Veréb, Klára Megyeri

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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 2 institutions in 1 country.

Áron DernovicsDepartment of Medical Microbiology, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 10., H-6720 Szeged, Hungary.
György SeprényiDepartment of Anatomy, Histology and Embryology, Albert Szent-Györgyi Medical School, University of Szeged, Kossuth L. sgt. 40., H-6724 Szeged, Hungary.
Zsolt RázgaDepartment of Pathology, University of Szeged, Állomás u. 2, H-6720 Szeged, Hungary.
Ferhan AyaydinHungarian Centre of Excellence for Molecular Medicine (HCEMM) Nonprofit Ltd., Római krt. 21., H-6723 Szeged, Hungary.ORCID 0000-0002-9126-0865
Zoltán VerébRegenerative Medicine and Cellular Pharmacology Laboratory, Department of Dermatology and Allergology, University of Szeged, Korányi Fasor 6, H-6720 Szeged, Hungary.
Klára MegyeriDepartment of Medical Microbiology, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 10., H-6720 Szeged, Hungary.
University of Szeged · HUHUN-REN Szegedi Biológiai Kutatóközpont · HU

Funding

European Regional Development Fund EFOP-3.6.1-16-2016-00008
6 · The paper itself

Abstract

backgroundPhenol-soluble modulins (PSMs) are pore-forming toxins (PFTs) produced by staphylococci. PSMs exert diverse cellular effects, including lytic, pro-apoptotic, pro-inflammatory and antimicrobial actions. Since the effects of PSMs on autophagy have not yet been reported, we evaluated the autophagic activity in HaCaT keratinocytes treated with recombinant PSMα3.

methodsThe autophagic flux and levels of autophagic marker proteins were determined using Western blot analysis. Subcellular localization of LC3B and Beclin-1 was investigated using an indirect immunofluorescence assay. The ultrastructural features of control and PSMα3-treated cells were evaluated via transmission electron microscopy. Cytoplasmic acidification was measured via acridine orange staining. Phosphorylation levels of protein kinases, implicated in autophagy regulation, were studied using a phospho-kinase array and Western blot analysis.

resultsPSMα3 facilitated the intracellular redistribution of LC3B, increased the average number of autophagosomes per cell, promoted the development of acidic vesicular organelles, elevated the levels of LC3B-II, stimulated autophagic flux and triggered a significant decrease in the net autophagic turnover rate. PSMα3 induced the accumulation of autophagosomes/autolysosomes, amphisomes and multilamellar bodies at the 0.5, 6 and 24 h time points, respectively. The phospho-Akt1/2/3 (T308 and S473), and phospho-mTOR (S2448) levels were decreased, whereas the phospho-Erk1/2 (T202/Y204 and T185/Y187) level was increased in PSMα3-treated cells.

conclusionsIn HaCaT keratinocytes, PSMα3 stimulates autophagy. The increased autophagic activity elicited by sub-lytic PSM concentrations might be an integral part of the cellular defense mechanisms protecting skin homeostasis.

Indexed as

autophagykeratinocytephenol-soluble modulinpore-forming toxinstaphylococci

Identifiers

PMID38002017
PMCPMC10669503
OpenAlexW4388567715

What Socratic holds

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LicenceCC BY
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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 Socratic graph.