Alternating magnetic fields drive stimulation of gene expression via generation of reactive oxygen species
Magnetogenetics represents a method for remote control of cellular function. Previous work suggests that generation of reactive oxygen species (ROS) initiates downstream signaling. Herein, a chemical biology approach was used to elucidate further the mechanism of radio frequency-alternating magnetic...
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Veröffentlicht in: | iScience 2024-03, Vol.27 (3), p.109186-109186, Article 109186 |
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Sprache: | eng |
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Zusammenfassung: | Magnetogenetics represents a method for remote control of cellular function. Previous work suggests that generation of reactive oxygen species (ROS) initiates downstream signaling. Herein, a chemical biology approach was used to elucidate further the mechanism of radio frequency-alternating magnetic field (RF-AMF) stimulation of a TRPV1-ferritin magnetogenetics platform that leads to Ca2+ flux. RF-AMF stimulation of HEK293T cells expressing TRPV1-ferritin resulted in ∼30% and ∼140% increase in intra- and extracellular ROS levels, respectively. Mutations to specific cysteine residues in TRPV1 responsible for ROS sensitivity eliminated RF-AMF driven Ca2+-dependent transcription of secreted embryonic alkaline phosphatase (SEAP). Using a non-tethered (to TRPV1) ferritin also eliminated RF-AMF driven SEAP production, and using specific inhibitors, ROS-activated TRPV1 signaling involves protein kinase C, NADPH oxidase, and the endoplasmic reticulum. These results suggest ferritin-dependent ROS activation of TRPV1 plays a key role in the initiation of magnetogenetics, and provides relevance for potential applications in medicine and biotechnology.
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•AMF activates TRPV1-ferritin magnetogenetics platform•AMF induces increased extra- and intracellular ROS levels•Localized ROS oxidizes crucial cysteine residues for channel activation•AMF stimulation involves PKC, NOX, ER, and gene transcription
Biological sciences; Molecular mechanism of gene regulation; Cell biology; |
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ISSN: | 2589-0042 2589-0042 |
DOI: | 10.1016/j.isci.2024.109186 |