Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: Molecular mechanism for cancer- and blood-brain barrier-related effects

Ischemia-reperfusion injuries, such as those suffered from various types of cardiovascular disease, are major causes of death and disability. For relatively short periods of ischemia, much of the damage is potentially reversible and in fact, does not occur until the influx of oxygen during the reperfusion stage. Because of this, there is a window of opportunity to protect the ischemic tissue. Here, we review several mechanisms of protection, such as heat shock proteins, opioids, collateral blood flow, and nitric oxide induction, and the evidence indicating that magnetic fields may be used as a means of providing protection via each of these mechanisms. While there are few studies demonstrating direct protection with magnetic field therapies, there are a number of published reports indicating that electromagnetic fields may be able to influence some of the biochemical systems with protective applications.

Section: Mechanisms: Heat Shock Proteinsmentioning

confidence: 99%

The influence of extremely low frequency magnetic fields on cytoprotection and repair

Robertson

Thomas

Bureau

et al. 2006

“…Cleary et al, 1997;Laszlo et al, 2005;Lim et al, 2005;Lantow et al, 2006;Chauhan et al, 2006a, b], except at high SARs where thermal effects are clearly implicated , and those where one or more HSPs appear to be induced [e.g. Kwee et al, 2001;Shallom et al, 2002;Leszczynski et al, 2002;Weisbrot et al, 2003;reviewed Belyaev, 2005]. Some of these latter reports involve up-regulation of the major inducible HSP70 chaperone, but others focus on the smaller HSP27 protein, whose orthologues are encoded by the hsp16 gene family in C.…”

Section: Introductionmentioning

confidence: 99%

“…Several reports have suggested that some (but not all) vertebrate cell lines may be sensitive to nonthermal effects of RF exposure. These include broad effects on the proteome and specifically on the expression of vimentin isoforms [Nylund & Leszczynski, 2004], as well as on the expression and phosphorylation of small heat-shock proteins (HSP27) in human endothelial cells [Leszczynski et al, 2002]. However, these changes are not seen in several other cell types .…”

Section: Introductionmentioning

confidence: 99%

Continuous wave and simulated GSM exposure at 1.8 W/kg and 1.8 GHz do not induce hsp16‐1 heat‐shock gene expression in Caenorhabditis elegans

Dawe¹,

Nylund²,

Leszczyński³

et al. 2007

Self Cite

Recent data suggest that there might be a subtle thermal explanation for the apparent induction by radiofrequency (RF) radiation of transgene expression from a small heat‐shock protein (hsp16‐1) promoter in the nematode, Caenorhabditis elegans. The RF fields used in the C. elegans study were much weaker (SAR 5–40 mW kg−1) than those routinely tested in many other published studies (SAR ∼2 W kg−1). To resolve this disparity, we have exposed the same transgenic hsp16‐1::lacZ strain of C. elegans (PC72) to higher intensity RF fields (1.8 GHz; SAR ∼1.8 W kg−1). For both continuous wave (CW) and Talk‐pulsed RF exposures (2.5 h at 25 °C), there was no indication that RF exposure could induce reporter expression above sham control levels. Thus, at much higher induced RF field strength (close to the maximum permitted exposure from a mobile telephone handset), this particular nematode heat‐shock gene is not up‐regulated. However, under conditions where background reporter expression was moderately elevated in the sham controls (perhaps as a result of some unknown co‐stressor), we found some evidence that reporter expression may be reduced by ∼15% following exposure to either Talk‐pulsed or CW RF fields. Bioelectromagnetics 29:92–99, 2008. © 2007 Wiley‐Liss, Inc.

“…Considered as nonthermal GSM-RFR effects, yet with power absorptions of >1 W/Kg, are influences on human skin fibroblast morphology and cell cycle related gene expression [Pacini et al, 2002], on human endothelial cell stress responses [Leszczynski et al, 2002], as well as on chicken embryo hsp70 expression and cytoprotection against hypoxia [Di Carlo et al, 2002]. At the frequency and power density tested in this study, GSM-like RFR seems to have influenced the regulation of the expression of critical morphogenetic factors, such as the BMP related genes, in newborn rat kidneys after exposure to this type of radiation during the early stages of embryonal development.…”

Section: Discussionmentioning

confidence: 99%

“…These include gene expression alteration of heat shock proteins, such as hsp70 [Di Carlo et al, 2002] and hsp27/p38MAPK [Leszczynski et al, 2002], early response genes like c-fos [Fritze et al, 1997;Goswami et al, 1999], as well as neurotransmitter production, concentration and localization [Mausset et al, 2001;Testylier et al, 2002]. Based on the above, RFR specific effects were suggested to induce or promote the development of cancer and other diseases [French et al, 2001;Leszczynski et al, 2002], a hypothesis not proven for any type of cancer [Heikkinen et al, 2001;Bartsch et al, 2002] and not proven for the proliferation of glioma cells [Stagg et al, 1997;Higashikubo et al, 2001].…”

Section: Introductionmentioning

confidence: 99%

Bone morphogenetic protein expression in newborn rat kidneys after prenatal exposure to radiofrequency radiation

Pyrpasopoulou

Kotoula

Cheva

et al. 2004

Effects of nonthermal radiofrequency radiation (RFR) of the global system of mobile communication (GSM) cellular phones have been as yet mostly studied at the molecular level in the context of cellular stress and proliferation, as well as neurotransmitter production and localization. In this study, a simulation model was designed for the exposure of pregnant rats to pulsed GSM-like RFR (9.4 GHz), based on the different resonant frequencies of man and rat. The power density applied was 5 mW/cm 2 , in order to avoid thermal electromagnetic effects as much as possible. Pregnant rats were exposed to RFR during days 1-3 postcoitum (p.c.) (embryogenesis, pre-implantation) and days 4-7 p.c. (early organogenesis, peri-implantation). Relative expression and localization of bone morphogenetic proteins (BMP) and their receptors (BMPR), members of a molecular family currently considered as major endocrine and autocrine morphogens and known to be involved in renal development, were investigated in newborn kidneys from RFR exposed and sham irradiated (control) rats. Semiquantitative duplex RT-PCR for BMP-4, -7, BMPR-IA, -IB, and -II showed increased BMP-4 and BMPR-IA, and decreased BMPR-II relative expression in newborn kidneys. These changes were statistically significant for BMP-4, BMPR-IA, and -II after exposure on days 1-3 p.c. (P <.001 each), and for BMP-4 and BMPR-IA after exposure on days 4-7 p.c. (P <.001 and P ¼.005, respectively). Immunohistochemistry and in situ hybridization (ISH) showed aberrant expression and localization of these molecules at the histological level. Our findings suggest that GSM-like RFR interferes with gene expression during early gestation and results in aberrations of BMP expression in the newborn. These molecular changes do not appear to affect renal organogenesis and may reflect a delay in the development of this organ. The differences of relative BMP expression after different time periods of exposure indicate the importance of timing for GSM-like RFR effects on embryonic development.