Weak power frequency magnetic fields induce microtubule cytoskeleton reorganization depending on the epidermal growth factor receptor and the calcium related signaling.

We have shown previously that a weak 50 Hz magnetic field (MF) invoked the actin-cytoskeleton, and provoked cell migration at the cell level, probably through activating the epidermal growth factor receptor (EGFR) related motility pathways. However, whether the MF also affects the microtubule (MT)-cytoskeleton is still unknown. In this article, we continuously investigate the effects of 0.

Developmental and cancer-associated plasticity of DNA replication preferentially targets GC-poor, lowly expressed and late-replicating regions.

The spatiotemporal program of metazoan DNA replication is regulated during development and altered in cancers. We have generated novel OK-seq, Repli-seq and RNA-seq data to compare the DNA replication and gene expression programs of twelve cancer and non-cancer human cell types. Changes in replication fork directionality (RFD) determined by OK-seq are widespread but more frequent within GC-poor isochores and largely disconnected from transcription changes.

Exposure to 50Hz-sinusoidal electromagnetic field induces DNA damage-independent autophagy.

As electromagnetic field (EMF) is commonly encountered within our daily lives, the biological effects of EMF are of great concern. Autophagy is a key process for maintaining cellular homeostasis, and it can also reveal cellular responses to environmental stimuli. In this study, we aim to investigate the biological effects of a 50Hz-sinusoidal electromagnetic field on autophagy and we identified its mechanism of action in Chinese Hamster Lung (CHL) cells.

Extremely low-frequency electromagnetic fields enhance the proliferation and differentiation of neural progenitor cells cultured from ischemic brains.

In the mammalian brain, neurogenesis persists throughout the embryonic period and adulthood in the subventricular zone of the lateral ventricle and the granular zone (dentate gyrus) of the hippocampus. Newborn neural progenitor cells (NPCs) in the two regions play a critical role in structural and functional plasticity and neural regeneration after brain injury. Previous studies have reported that extremely low-frequency electromagnetic fields (ELF-EMF) could promote osteogenesis, angiogenesis, and cardiac stem cells' differentiation, which indicates that ELF-EMF might be an effective tool for regenerative therapy.

Weak power frequency magnetic field acting similarly to EGF stimulation, induces acute activations of the EGFR sensitive actin cytoskeleton motility in human amniotic cells.

In this article, we have examined the motility-related effects of weak power frequency magnetic fields (MFs) on the epidermal growth factor receptor (EGFR)-sensitive motility mechanism, including the F-actin cytoskeleton, growth of invasive protrusions and the levels of signal molecules in human amniotic epithelial (FL) cells. Without extracellular EGF stimulation, the field stimulated a large growth of new protrusions, especially filopodia and lamellipodia, an increased population of vinculin-associated focal adhesions. And, an obvious reduction of stress fiber content in cell centers was found, corresponding to larger cell surface areas and decreased efficiency of actin assembly of FL cells in vitro, which was associated with a decrease in overall F-actin content and special distributions.

[Effects of 50 Hz sinusoidal magnetic field on Ca2+ release channel ryanodine receptor of sarcoplasmic reticulum vesicles].

Objective: To investigate the effects of sinusoidal magnetic field on isolated sarcoplasmic reticulum (SR) calcium release channel (RyR1) function.

Methods: With the Ca2+ dynamic spectrum and isotope labeled methods, the Ca2+ release and [(3)H]-Ryanodine binding, the initial rates of NADH oxidation and the production of superoxide of SR exposed to 50 Hz sinusoidal magnetic field (MF) were investigated respectively.

Results: 0.

Selenoprotein N is required for ryanodine receptor calcium release channel activity in human and zebrafish muscle.

Mutations affecting the seemingly unrelated gene products, SepN1, a selenoprotein of unknown function, and RyR1, the major component of the ryanodine receptor intracellular calcium release channel, result in an overlapping spectrum of congenital myopathies. To identify the immediate developmental and molecular roles of SepN and RyR in vivo, loss-of-function effects were analyzed in the zebrafish embryo. These studies demonstrate the two proteins are required for the same cellular differentiation events and are needed for normal calcium fluxes in the embryo.

[Effect of 50 Hz power frequency magnetic field on microfilament cytoskeleton assembly of human amnion FL cells].

Objective: Investigations were carried out to understand the effect of 50 Hz power frequency magnetic field on microfilament assembly of human amniotic cells and on expression of actin and epidermal growth factor receptor.

Methods: Human amnion FL cells were exposed to 0.1, 0.

Non-thiol reagents regulate ryanodine receptor function by redox interactions that modify reactive thiols.

The Ca(2+) release channel (CRC) from sarcoplasmic reticulum (SR) is rich in thiol groups, and their oxidation/- reduction by thiol reagents activates/inhibits the CRC. Most channel regulators are not thiol reagents, and the mechanism of their action is illusive. Here the authors show that many channel activators act as electron acceptors, while many channel inhibitors act as electron donors in free radical reactions.

EGF receptor clustering is induced by a 0.4 mT power frequency magnetic field and blocked by the EGF receptor tyrosine kinase inhibitor PD153035.

Atomic force microscopy (AFM), transmission electron microscopy (TEM), and confocal laser scanning microscopy were used to investigate the effects of a 50 Hz 0.4 mT magnetic field (MF) on the clustering of purified epidermal growth factor receptors (EGFRs) and EGFRs in Chinese hamster lung (CHL) cell membrane. The results demonstrate that exposing purified EGFRs to the MF for 30 min induces receptor clustering.

[Effects of power frequency magnetic field on Ca2+ transport of skeletal muscle sarcoplasmic reticulum vesicles].

Objective: To investigate the effects of power frequency magnetic field on the Ca2+ transport dynamics of isolated sarcoplasmic reticulum vesicles.

Methods: The assays of Ca2+ uptake time course and the Ca2+-ATPase activity of sarcoplasmic reticulum vesicles were investigated by using dynamic mode of spectrometry with a Ca2+ dye; Ca2+ release channel activation was examined by 3H-ryanodine binding and Ca2+ release assays; membrane fluidity of sarcoplasmic reticulum vesicles was examined by fluorescence polarization, without or with exposure to the vesicles at a 0.4 mT, 50 Hz sinusoidal magnetic field.

Pulsed electric field exposure of insulin induces anti-proliferative effects on human hepatocytes.

The purpose of this study was to examine the effects and the mechanism of a pulsed electric field (PEF) on insulin and its subsequent mediation of proliferative changes in human hepatocytes in vitro. The PEF, the electric field intensity coupled into the culture medium, was about 0.7 V/m with a repeating frequency of 50 Hz.

[Raman analysis of conformation changes of insulin solvent after being exposed to ELF pulsed electric field].

Raman spectra of insulin solvents are presented before and after being exposed to the pulsed electric field with extremely low frequency 50 Hz (ELF). The covalences of the molecule were not affected and the changes of some secondary bonds such as hydrogen bonds and salt bonds were observed. Detailed analysis of these spectra indicates that the alpha-helix of insulin molecule was destroyed after the exposure, which is proved by the shift of the peak of the amide I region toward higher wave number and by the appearance of several new peaks: 1561 and 1594 cm(-1).

Selenium compounds modulate the calcium release channel/ryanodine receptor of rabbit skeletal muscle by oxidizing functional thiols.

Selenium compounds, such as sodium selenite and Ebselen were shown to increase high affinity ryanodine binding to the skeletal muscle type ryanodine receptor (RyR1) at nanomolar concentrations, and inhibit the receptor at low micromolar concentrations. This biphasic response was observed in both concentration and time-dependent assays. Extensive washing did not reverse either the stimulation or suppression of receptor binding, but both were prevented or reversed by addition of reduced glutathione, GSH.

Effect of intermittent and continuous hypoxia on ryanodine receptors of rat heart.

Intermittent hypoxia (IH) adaptation has been shown to exert beneficial effects on the functions of hearts that had been subjected to insult by ischemia or ischemia/reperfusion. To understand whether calcium release channels/ryanodine receptors (RyRs) were involved, the effects of IH and continuous hypoxia (CH) on [3H]ryanodine binding to homogenates of rat hearts were investigated. Similar studies were performed on rat skeletal muscle.

Modulation of the interactions of isolated ryanodine receptors of rabbit skeletal muscle by Na+ and K+.

Ryanodine receptors (RyRs) of skeletal muscle, as calcium release channels, have been found to form semicrystalline arrays in the membrane of sarcoplasmic reticulum. Recently, both experimental observations and theoretical simulations suggested cooperative coupling within interlocking RyRs. To better understand the interactions between RyRs and their modulation, the aggregation and dissociation of isolated RyRs in aqueous medium containing various Na(+) and K(+) concentrations were investigated using photon correlation spectroscopy (PCS) and atomic force microscopy (AFM).

Skeletal muscle sarcoplasmic reticulum contains a NADH-dependent oxidase that generates superoxide.

Skeletal muscle sarcoplasmic reticulum (SR) is shown to contain an NADH-dependent oxidase (NOX) that reduces molecular oxygen to generate superoxide. Its activity is coupled to an activation of the Ca2+ release mechanism, as evident by stimulation in the rate of high-affinity ryanodine binding. NOX activity, coupled to the production of superoxide, is not derived from the mitochondria but is SR in origin.