ArticleJournal of bioenergetics and biomembranes2026
EMF-induced mesenchymal stem cell migration is mediated by SOCE-dependent calcium influx and modulated by ROCK signaling.
Article in Journal of bioenergetics and biomembranes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Corrections and comments
- Erratum issued
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5 authors.
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Abstract
Electromagnetic field (EMF) exposure promotes mesenchymal stem cell (MSCs) migration, a critical process in regenerative medicine. While calcium (Ca²⁺) signaling is implicated, the primary Ca²⁺ entry pathway and its downstream mechanisms remain elusive. This study investigates the hypothesis that store-operated calcium entry (SOCE) serves as a major Ca²⁺ influx mechanism and modulates the ROCK pathway to drive EMF-induced MSCs migration. Rat bone marrow-derived MSCs were exposed to a 50 Hz, 5 mT sinusoidal EMF. Cell migration was assessed via Transwell assays. Intracellular Ca²⁺ and SOCE activity were measured using Fluo-4 AM. Transcriptomic profiling was performed by RNA sequencing. Cytoskeletal reorganization (F-actin, acetylated α-tubulin) and protein expression (Orai1, ROCK1/2) were analyzed by immunofluorescence and western blotting, using pharmacological inhibitors (BTP2 for SOCE, Y-27632 for ROCK) and calcium chelators to dissect the pathway. EMF exposure significantly enhanced MSCs migration and activated calcium signaling pathways. This pro-migratory effect was strictly dependent on extracellular Ca²⁺ influx and was abolished by SOCE inhibition with BTP2. EMF upregulated the SOCE channel Orai1 and enhanced SOCE activity. Crucially, EMF suppressed ROCK1/2 expression under normal conditions, but this suppression was not reversed under SOCE inhibition or in low-calcium medium and EMF exposure increased ROCK1/2 expression in Ca²⁺-free medium (with 2 mM EGTA). SOCE inhibition also attenuated EMF-induced cytoskeletal reorganization, including perinuclear accumulation of acetylated α-tubulin and F-actin polymerization. Our findings establish SOCE-mediated Ca²⁺ influx as the critical driver of EMF-promoted MSCs migration. This process involves the upregulation of Orai1 and elicits a biphasic, context-dependent modulation of the ROCK pathway. The pro-migratory phenotype requires the synergy of SOCE-dependent Ca²⁺ influx and ROCK downregulation, leading to coordinated cytoskeletal remodeling. This study redefines the mechanistic understanding of EMF bioeffects, highlighting SOCE as a key regulator that integrates calcium signaling with cytoskeletal dynamics to control cell migration.
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