| Records |
Author  |
Zuo, H.; Lin, T.; Wang, D.; Peng, R.; Wang, S.; Gao, Y.; Xu, X.; Zhao, L.; Wang, S.; Su, Z. |
| Title |
RKIP Regulates Neural Cell Apoptosis Induced by Exposure to Microwave Radiation Partly Through the MEK/ERK/CREB Pathway |
Type |
Journal Article |
| Year |
2014 |
Publication |
Molecular neurobiology |
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| Keywords |
apoptosis; creb pathway; erk; mek; microwave radiation; pc12 cells; rkip |
| Abstract |
In the present study, we investigated whether Raf-1 kinase inhibitory protein (RKIP) is important for neural cell apoptosis induced by microwave exposure and explored the role of MEK/ERK/CREB pathway regulated by RKIP in the apoptosis. Differentiated PC12 cells were exposed to continuous microwave radiation at 2.856 GHz for 5 min with average power density of 30 mW/cm(2). RKIP sense and anti-sense recombinant plasmids were constructed and transfected into PC12 cells, respectively. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining and caspase-3 activity assay were used to detect cell apoptosis. The results showed that RKIP was downregulated after microwave exposure while the MEK/ERK/CREB signaling pathway was activated excessively. Moreover, the ratio of Bcl-2/Bax decreased, activity of caspase-3 increased, and thus apoptotic DNA fragmentation increased. RKIP overexpression significantly inhibited the phosphorylation of MEK, ERK, and CREB, while RKIP downregulation had the reverse effect. Furthermore, U0126 was found to antagonize the changes caused by RKIP downregulation after exposure to radiation. In conclusion, RKIP plays an important role in the neural cell apoptosis induced by microwave radiation, and the regulation of cell apoptosis by RKIP is partly through the MEK/ERK/CREB pathway. This suggests that RKIP may act as a key regulator of neuronal damage caused by microwave radiation. |
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WP5 In vitro |
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UNIBAS @ david.schuermann @ |
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556 |
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Zoppetti, N.; Andreuccetti, D.; Bellieni, C.; Bogi, A.; Pinto, I. |
| Title |
Evaluation and characterization of fetal exposures to low frequency magnetic fields generated by laptop computers |
Type |
Journal Article |
| Year |
2011 |
Publication |
Progress in Biophysics and Molecular Biology |
Abbreviated Journal |
Prog Biophys Mol Biol |
| Volume |
107 |
Issue |
3 |
Pages |
456-463 |
| Keywords |
*Computers; Electric Power Supplies; Female; *Fetus; Humans; *Magnetic Fields/adverse effects; *Maternal Exposure/adverse effects; Pregnancy; Radiometry |
| Abstract |
Portable – or “laptop” – computers (LCs) are widely and increasingly used all over the world. Since LCs are often used in tight contact with the body even by pregnant women, fetal exposures to low frequency magnetic fields generated by these units can occur. LC emissions are usually characterized by complex waveforms and are often generated by the main AC power supply (when connected) and by the display power supply sub-system. In the present study, low frequency magnetic field emissions were measured for a set of five models of portable computers. For each of them, the magnetic flux density was characterized in terms not just of field amplitude, but also of the so called “weighted peak” (WP) index, introduced in the 2003 ICNIRP Statement on complex waveforms and confirmed in the 2010 ICNIRP Guidelines for low frequency fields. For the model of LC presenting the higher emission, a deeper analysis was also carried out, using numerical dosimetry techniques to calculate internal quantities (current density and in-situ electric field) with reference to a digital body model of a pregnant woman. Since internal quantities have complex waveforms too, the concept of WP index was extended to them, considering the ICNIRP basic restrictions defined in the 1998 Guidelines for the current density and in the 2010 Guidelines for the in-situ electric field. Induced quantities and WP indexes were computed using an appropriate original formulation of the well known Scalar Potential Finite Difference (SPFD) numerical method for electromagnetic dosimetry in quasi-static conditions. |
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CNR, Institute of Applied Physics Nello Carrara (IFAC-CNR), Sesto Fiorentino (FI), Italy. n.zoppetti@ifac.cnr.it |
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English |
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0079-6107 |
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WP2 Exposure measurements |
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PMID:22019904 |
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CNR-ISIB @ paolo.ravazzani @ |
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223 |
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Zoltowski, B.D.; Gardner, K.H. |
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Tripping the light fantastic: blue-light photoreceptors as examples of environmentally modulated protein-protein interactions |
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Journal Article |
| Year |
2011 |
Publication |
Biochemistry |
Abbreviated Journal |
Biochemistry |
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50 |
Issue |
1 |
Pages |
4-16 |
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Animals; Bacteria/chemistry/metabolism; Bacterial Proteins/chemistry/*metabolism; Biotechnology; Cryptochromes/chemistry/*metabolism; Flavoproteins/chemistry/*metabolism; Halorhodospira halophila/chemistry/metabolism; Humans; Light; Models, Molecular; Photochemical Processes; Photoreceptor Cells/chemistry/*metabolism; Photoreceptors, Microbial/chemistry/*metabolism; Protein Interaction Maps; Protein Structure, Tertiary; Signal Transduction |
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Blue-light photoreceptors play a pivotal role in detecting the quality and quantity of light in the environment, controlling a wide range of biological responses. Several families of blue-light photoreceptors have been characterized in detail using biophysics and biochemistry, beginning with photon absorption, through intervening signal transduction, to regulation of biological activities. Here we review the light oxygen voltage, cryptochrome, and sensors of blue light using FAD families, three different groups of proteins that offer distinctly different modes of photochemical activation and signal transduction yet play similar roles in a vast array of biological responses. We cover mechanisms of light activation and propagation of conformational responses that modulate protein-protein interactions involved in biological signaling. Discovery and characterization of these processes in natural proteins are now allowing the design of photoregulatable engineered proteins, facilitating the generation of novel reagents for biochemical and cell biological research. |
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Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8816, United States |
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0006-2960 |
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PMID:21141905 |
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no |
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IT'IS @ evaj @ |
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248 |
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Zimmerman, J.W.; Pennison, M.J.; Brezovich, I.; Yi, N.; Yang, C.T.; Ramaker, R.; Absher, D.; Myers, R.M.; Kuster, N.; Costa, F.P.; Barbault, A.; Pasche, B. |
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Cancer cell proliferation is inhibited by specific modulation frequencies |
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Journal Article |
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2012 |
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British Journal of Cancer |
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Br J Cancer |
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106 |
Issue |
2 |
Pages |
307-313 |
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0007-0920 |
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IT'IS @ evaj @ |
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441 |
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Zhu, H.; Wang, J.; Cui, J.; Fan, X. |
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Effects of extremely low frequency electromagnetic fields on human fetal scleral fibroblasts |
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Journal Article |
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2014 |
Publication |
Toxicology and industrial health |
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August |
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collagen type i; extremely low frequency electromagnetic; fibroblast; field; matrix metalloproteinase-2; sclera; transforming growth factor beta-2 |
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This study investigated the effects of extremely low frequency electromagnetic fields (ELF-EMFs) on human fetal scleral fibroblasts (HFSFs). HFSFs were subjected to 50 Hz artificial ELF-EMFs generated by Helmholtz coils with 0.1, 0.2, 0.5, and 1.0 mT field intensities for 6 to 48 h. The viability and factors involved in scleral structuring of HFSFs were determined. The growth rate of HFSFs significantly decreased after only 24 h of exposure to ELF-EMFs (0.2 mT). The messenger RNA (mRNA) expression of collagen type I (COL1A1) decreased and expression of matrix metalloproteinase-2 (MMP-2) increased significantly. There was a decrease in tissue inhibitor of MMP-2 mRNA levels between treated and control cells only at the 1.0 mT intensity level. Transforming growth factor beta-2 mRNA increased in exposed cells, and, simultaneously, fibroblast growth factor-2 mRNA levels decreased. The protein expressions of COL1A1 and MMP-2 were also significantly altered subsequent to exposure (p < 0.05). This study shows that ELF-EMFs had biological effects on HFSFs and could cause abnormality in scleral collagen. |
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WP5 In vitro |
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UNIBAS @ david.schuermann @ |
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629 |
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