Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
BioIonic Currents Electromagnetic Pulsing Systems (BICEPS) Laboratory, National University of Singapore, Singapore.
FASEB J. 2019 Nov;33(11):12853-12872. doi: 10.1096/fj.201900057R. Epub 2019 Sep 13.
We show that both supplemental and ambient magnetic fields modulate myogenesis. A lone 10 min exposure of myoblasts to 1.5 mT amplitude supplemental pulsed magnetic fields (PEMFs) accentuated myogenesis by stimulating transient receptor potential (TRP)-C1-mediated calcium entry and downstream nuclear factor of activated T cells (NFAT)-transcriptional and P300/CBP-associated factor (PCAF)-epigenetic cascades, whereas depriving myoblasts of ambient magnetic fields slowed myogenesis, reduced TRPC1 expression, and silenced NFAT-transcriptional and PCAF-epigenetic cascades. The expression levels of peroxisome proliferator-activated receptor γ coactivator 1α, the master regulator of mitochondriogenesis, was also enhanced by brief PEMF exposure. Accordingly, mitochondriogenesis and respiratory capacity were both enhanced with PEMF exposure, paralleling TRPC1 expression and pharmacological sensitivity. Clustered regularly interspaced short palindromic repeats-Cas9 knockdown of TRPC1 precluded proliferative and mitochondrial responses to supplemental PEMFs, whereas small interfering RNA gene silencing of TRPM7 did not, coinciding with data that magnetoreception did not coincide with the expression or function of other TRP channels. The aminoglycoside antibiotics antagonized and down-regulated TRPC1 expression and, when applied concomitantly with PEMF exposure, attenuated PEMF-stimulated calcium entry, mitochondrial respiration, proliferation, differentiation, and epigenetic directive in myoblasts, elucidating why the developmental potential of magnetic fields may have previously escaped detection. Mitochondrial-based survival adaptations were also activated upon PEMF stimulation. Magnetism thus deploys an authentic myogenic directive that relies on an interplay between mitochondria and TRPC1 to reach fruition.-Yap, J. L. Y., Tai, Y. K., Fröhlich, J., Fong, C. H. H., Yin, J. N., Foo, Z. L., Ramanan, S., Beyer, C., Toh, S. J., Casarosa, M., Bharathy, N., Kala, M. P., Egli, M., Taneja, R., Lee, C. N., Franco-Obregón, A. Ambient and supplemental magnetic fields promote myogenesis a TRPC1-mitochondrial axis: evidence of a magnetic mitohormetic mechanism.
我们证明了补充磁场和环境磁场都可以调节成肌作用。将成肌细胞单独暴露于 1.5 mT 幅度的补充脉冲磁场 (PEMF) 10 分钟，通过刺激瞬时受体电位 (TRP)-C1 介导的钙内流以及下游核因子活化 T 细胞 (NFAT)-转录和 P300/CBP 相关因子 (PCAF)-表观遗传级联，增强成肌作用，而剥夺成肌细胞的环境磁场则会减缓成肌作用，降低 TRPC1 的表达，并沉默 NFAT-转录和 PCAF-表观遗传级联。过氧化物酶体增殖物激活受体 γ 共激活因子 1α的表达水平也被短暂的 PEMF 暴露增强，该因子是线粒体发生的主要调节因子。因此，PEMF 暴露增强了线粒体发生和呼吸能力，与 TRPC1 的表达和药物敏感性相平行。TRPC1 的 CRISPR/Cas9 敲低排除了补充 PEMF 对增殖和线粒体的反应，而 TRPM7 的小干扰 RNA 基因沉默则没有，这与磁受体与其他 TRP 通道的表达或功能不重合的数据一致。氨基糖苷类抗生素拮抗并下调 TRPC1 的表达，当与 PEMF 暴露同时应用时，会减弱 PEMF 刺激的钙内流、线粒体呼吸、增殖、分化和成肌细胞中的表观遗传指令，阐明了为什么磁场的发育潜力以前可能未被发现。PEMF 刺激还激活了基于线粒体的生存适应。因此，磁场利用了线粒体和 TRPC1 之间的相互作用来发挥其真正的成肌作用，从而实现了磁导向。-Yap，J. L. Y.，Tai，Y. K.，Fröhlich，J.，Fong，C. H. H.，Yin，J. N.，Foo，Z. L.，Ramanan，S.，Beyer，C.，Toh，S. J.，Casarosa，M.，Bharathy，N.，Kala，M. P.，Egli，M.，Taneja，R.，Lee，C. N.，Franco-Obregón，A. 环境磁场和补充磁场促进成肌作用：TRPC1-线粒体轴：磁促线粒体机制的证据。
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