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Updated: Jul 10, 2025
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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
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Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes
Áron Dernovics1, György Seprényi2, Zsolt Rázga3
1Department of Medical Microbiology, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 10., H-6720 Szeged, Hungary.
Biomedicines
|November 25, 2023
Summary
Staphylococcus aureus phenol-soluble modulin alpha3 (PSMα3) stimulates autophagy in skin cells. This increased autophagic activity may be a defense mechanism to maintain skin homeostasis.
Area of Science:
- Cell Biology
- Microbiology
- Immunology
Background:
- Phenol-soluble modulins (PSMs) are pore-forming toxins produced by staphylococci.
- PSMs have diverse cellular effects, including lytic, pro-apoptotic, pro-inflammatory, and antimicrobial actions.
- The impact of PSMs on autophagy remains largely unexplored.
Purpose of the Study:
- To investigate the effects of recombinant PSMα3 on autophagic activity in HaCaT keratinocytes.
- To elucidate the role of PSMα3 in cellular defense mechanisms.
Main Methods:
- Western blot analysis to assess autophagic flux and marker proteins (LC3B).
- Indirect immunofluorescence assay for LC3B and Beclin-1 localization.
- Transmission electron microscopy for ultrastructural analysis.
- Acridine orange staining for cytoplasmic acidification.
- Phospho-kinase array and Western blot to study signaling pathways.
Main Results:
- PSMα3 treatment increased autophagosome formation and acidic vesicular organelles.
- Elevated LC3B-II levels and stimulated autophagic flux were observed.
- PSMα3 induced accumulation of autophagosomes, amphisomes, and multilamellar bodies.
- Decreased phospho-Akt and phospho-mTOR, with increased phospho-Erk1/2 levels.
Conclusions:
- PSMα3 significantly stimulates autophagy in HaCaT keratinocytes.
- Enhanced autophagy by PSMα3 may represent a cellular defense mechanism.
- This process could contribute to maintaining skin homeostasis.
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