Effects of mobile phone electromagnetic radiation on rat hippocampus proteome
Ontology highlight
ABSTRACT:
INSTRUMENT(S): LTQ Orbitrap Velos
ORGANISM(S): Rattus Norvegicus (ncbitaxon:10116)
SUBMITTER: 
Dr. Ranjan Kumar Nanda
PROVIDER: MSV000084746 | MassIVE | Fri Jan 03 02:59:00 GMT 2020
REPOSITORIES: MassIVE
Similar Datasets
Project description:Worldwide, number of mobile phone users have increased from 5.57 billion in 2011 to 6.8 billion in 2019. However short and long term impacts of the electromagnetic radiations emitting of mobile phone on tissue homeostasis with particular to brain proteome composition needs further investigation. In this study, we attempted a global proteome profiling study of rat hippocampus exposed to mobile phone radiation for 20 weeks (for 3 hrs/day for 5 days/week) to identify deregulated proteins and western blot analysis for validation. As a result, we identified 358 hippocampus proteins, of which 16 showed deregulation (log2 (exposed/control), p-value<0.05). Majority of these deregulated proteins grouped to three clusters sharing similar molecular functions/pathways. A set of four proteins (Aldehyde dehydrogenase:Aldh5a1, Na+ K+ transporting ATPase:Atp1b2, plasma membrane calcium transporting ATPase:PMCA and protein S100b) presenting each functional pathways were selected as important molecules. Western blot analysis of this protein set, expect Atp1b2, in independent samples corroborated the mass spectrometry findings. Aldh5a1 involve in cellular energy metabolism, both Atp1b2 and PMCA responsible for membrane transport and protein S100b has neuroprotective role. In conclusion, we present deregulated hippocampus proteome upon mobile phone radiation which might impact healthy functioning of brain.
2019-12-20 | MSV000084731 | MassIVE
Project description:Worldwide, number of mobile phone users have increased from 5.57 billion in 2011 to 6.8 billion in 2019. However short and long term impacts of the electromagnetic radiations emitting of mobile phone on tissue homeostasis with particular to brain proteome composition needs further investigation. In this study, we attempted a global proteome profiling study of rat hippocampus exposed to mobile phone radiation for 20 weeks (for 3 hrs/day for 5 days/week) to identify deregulated proteins and western blot analysis for validation. As a result, we identified 358 hippocampus proteins, of which 16 showed deregulation (log2 (exposed vs control). Majority of these deregulated proteins grouped to three clusters sharing similar molecular functions/pathways. A set of four proteins (Aldehyde dehydrogenase:Aldh5a1, Na+ K+ transporting ATPase:Atp1b2, plasma membrane calcium transporting ATPase:PMCA and protein S100b) presenting each functional pathways were selected as important molecules. Western blot analysis of this protein set, expect Atp1b2, in independent samples corroborated the mass spectrometry findings. Aldh5a1 involve in cellular energy metabolism, both Atp1b2 and PMCA responsible for membrane transport and protein S100b has neuroprotective role. In conclusion, we present deregulated hippocampus proteome upon mobile phone radiation which might impact healthy functioning of brain.
2019-12-20 | MSV000084732 | MassIVE
Project description:Worldwide, number of mobile phone users have increased from 5.57 billion in 2011 to 6.8 billion in 2019. However short and long term impacts of the electromagnetic radiations emitting of mobile phone on tissue homeostasis with particular to brain proteome composition needs further investigation. In this study, we attempted a global proteome profiling study of rat hippocampus exposed to mobile phone radiation for 20 weeks (for 3 hrs/day for 5 days/week) to identify deregulated proteins and western blot analysis for validation. As a result, we identified 358 hippocampus proteins, of which 16 showed deregulation (log2 (exposed/control)>±1.0, p-value<0.05). Majority of these deregulated proteins grouped to three clusters sharing similar molecular functions/pathways. A set of four proteins (Aldehyde dehydrogenase:Aldh5a1, Na+ K+ transporting ATPase:Atp1b2, plasma membrane calcium transporting ATPase:PMCA and protein S100b) presenting each functional pathways were selected as important molecules. Western blot analysis of this protein set, expect Atp1b2, in independent samples corroborated the mass spectrometry findings. Aldh5a1 involve in cellular energy metabolism, both Atp1b2 and PMCA responsible for membrane transport and protein S100b has neuroprotective role. In conclusion, we present deregulated hippocampus proteome upon mobile phone radiation which might impact healthy functioning of brain.
2019-11-08 | MSV000084559 | MassIVE
Project description:Hippocampal lipidome and transcriptome profiling alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation
| PRJNA360284 | ENA
Project description:This model is from the article:
An old paper revisited: ‘‘A mathematical model of carbohydrate energy
metabolism. Interaction between glycolysis, the Krebs cycle and the
H-transporting shuttles at varying ATPases load’’ by V.V. Dynnik,
R. Heinrich and E.E. Sel’kov
Nazaret C, Mazat JP. J Theor Biol
2008 Jun;252(3):520-9. 18304584
,
Abstract:
We revisit an old Russian paper by V.V. Dynnik, R. Heinrich and E.E. Sel’kov (1980a, b) describing: ‘‘A mathematical model of
carbohydrate energy metabolism. Interaction between glycolysis, the Krebs cycle and the H-transporting shuttles at varying ATPases
load’’. We analyse the model mathematically and calculate the control coefficients as a function of ATPase loads. We also evaluate the
structure of the metabolic network in terms of elementary flux modes.
We show how this model can respond to an ATPase load as well as to the glucose supply. We also show how this simple model can
help in understanding the articulation between the major blocks of energetic metabolism, i.e. glycolysis, the Krebs cycle and the
H-transporting shuttles.
Note:
"dynnik_v1.xml":
created directly from "heinrich.sci" model file provided by Christine Nazaret
IDs changed to as per the paper
initial conditions set to steady state
results of Fig. 3 may be reproduced by running a a parameter scan over b15 in COPASI
"dynnik_v2.xml":
rescaled species such as s2_e1 = s2 * e1
are introduced whose evolution may be described through reaction participation, rather than via ODEs
original variables are retained as global parameters
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1202170000 | BioModels
Project description:Radiotherapy is an important therapeutic option for the treatment of primary and metastatic brain tumors, and there is increasing concern about the side effects associated with it as survival time after treatment increases. By far, cognitive dysfunction is the most common radiation-induced central nervous system injury. Studies have shown that the hippocampus is involved in radiation-induced cognitive dysfunction. We constructed a model of radiation-induced cognitive dysfunction by irradiating the whole brain of one-month-old rats with 20 Gy, and analyzed the expression profiles in the hippocampus of rats with radiation-induced cognitive dysfunction using single-cell RNA sequencing (scRNA-seq).
2023-12-12 | GSE249426 | GEO
Project description:Metagenomics of samples extracted from mobile phone surfaces via NextSeq 500 High OutputV2 Pair end Sequencing
| PRJDB13455 | ENA
Project description:The widespread use of wireless devices during the last decades is rising the concern about the adverse health effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted from these devices. Studies are targeting on unrevealing the underlying mechanisms of RF-EMR action. The contribution of the “omics” high throughput approaches is a prerequisite towards this direction. In the present work, C57BL/6 adult male mice were sham-exposed (nSE=8) or whole-body exposed (nExp=8) for 2h to GSM 1800 MHz mobile phone radiation at 11 V/m average electric field intensity, and the RF-EMR effects on the hippocampal lipidome and transcriptome profile were evaluated. The data analysis of the phospholipids’ fatty acid residues revealed that the levels of six fatty acids (16:0, 16:1 6+7c, 18:1 9c, 20:5 w3, SFA, MUFA) were significantly altered (p<0.05) in the exposed group. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p<0.05) between the two groups with a fold change cut off of 1.5. In general, the observed changes point out the attention to a membrane remodeling response of the tissue phospholipids after non-ionizing radiation exposure, reducing the Saturated Fatty Acids (SFA) and EPA omega-3 (20:5 w3) and increasing Monounsaturated Fatty Acids (MUFA) residues and in parallel reflect an impact to genes implicated in critical biological processes, as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism and cancer
2017-07-10 | GSE93199 | GEO
Project description:Glaucoma is not only the second leading cause of blindness worldwide, but patient numbers will also increase significantly in the coming years due to aging societies. Glaucoma is a progressive optic neuropathy with changes at the optic nerve head, gradual retinal ganglion cell (RGC) death, and visual field loss [1]. Unfortunately, glaucoma can remain asymptomatic until it is rather far progressed, hence about 10-50 % of patients are unaware they suffer from this disease. High intraocular pressure (IOP) is the main risk factor; however, normal-tension glaucoma (NTG) occurs in patients with physiological IOP [2]. This form account for about 30 % of glaucoma patients [3]. Furthermore, sustained IOP lowering can slow down, but does not completely stop disease progression in patients. [4, 5]. Additionally, the administration of topical glaucoma medications can lead to side effects, such as ocular irritation, decreasing the compliance of patients. These facts emphasize the importance of discovering new treatment strategies. The exact pathogenesis for glaucoma is still unknown, but several factors are considered to be involved (fig.1). The most prominent factor is an elevated IOP, which can cause blockade of axonal protein transport at the lamina cribrosa, causing an initial axonal damage and RGC death by trophic insufficiency. In addition, ischemic/hypoxic damage [6], astrocyte and glia cell alterations, and excessive stimulation of the glutamatergic system [7] are discussed as possible pathomechanisms. Moreover, an involvement of the immune system is considered [8-10]. In glaucoma patients, up- and downregulations in the systemic and ocular antibody profile were detected [11-13]. Also, antibody deposits were observed in glaucomatous retinae [14]. It is likely that a combination of several pathogenic factors/mechanisms increases the possibility of developing glaucoma. For the investigation of pathomechanisms and novel therapies, it is necessary to have suitable models that allow such screening. To investigate whether antibodies detected in glaucoma patients are part of glaucoma pathogenesis or a result of disease progression, the experimental autoimmune glaucoma (EAG) animal model was established. This animal model is based on the fact that autoantibodies against S100B, a small calcium binding protein expressed in glia cells, were found to be increased in glaucoma patients [15]. In this model, an immunization with S100B led to a significant loss of RGCs after 28 days and a fast degeneration of optic nerves [20]. The IOP in this model was not altered. Therefore, we were able to mimic the effects seen in NTG patients, an IOP-independent glaucomatous degeneration, by immunizing rats with S100B. S100B is a calcium-binding protein. In the central nervous system (CNS), it is mainly expressed by glial cells such as oligodendrocytes, Schwann cells, ependymal cells, retinal Müller cells and astrocytes [16]. S100B regulates and maintains the homeostasis of the important second messenger calcium and is therefore involved in many cell activities, such as signal transduction, cell differentiation, regulation of cell motility, transcription and cell cycle processes [17, 18]. Extracellularly, S100B can act as a signal molecule and bind receptors such as the receptor for advanced glycation end products (RAGE). In high concentrations, S100B can have negative effects and lead to cell death. For example, the binding of RAGE can induce the activation of microglia cells leading to a release of proinflammatory cytokines to an excessive extent [19]. Furthermore, there seems to be a link between S100B and neuronal diseases. In glaucoma patients, high antibody titers against S100B were found [20]. To investigate the effect of S100B in glaucoma more precisely, the immunization with S100B leads to a loss of retinal ganglion cells (RGCs) without an elevation of the IOP after 28 days in the EAG model [21, 22]. The goal of the present study was to detect the retinal biomarkers in EAG animals 7 and 14 days after immunization with S100B. To detect these new markers in disease development, a label free quantitative mass spectrometry-based approach will be used.
2022-02-16 | PXD023995 | Pride
Project description:The human neuroblastoma cell line Lan5 cells were cultured in complete DMEM till 80% confluence, then placed at 60000 cells per squared cm. Cells were then plated in 24-well plates for cell viability assay and in T75 flasks for RNA isolation. Medium was replaced with serum-free fresh medium for 12 hours prior to s100b treatment. Gene expression patterns were then analysed using the Human Focus Genechip array. In this study we analyze gene expression patterns in Lan5 cells treated with s100b protein. We utilized control cells (untreated) and two different concentrations (0.5 nM and 5 uM) of s100b. We used three biological replicates, for the three concentration tested, according to MIAME guidelines (total 9 chips were used in this study).
2010-06-08 | E-GEOD-15218 | biostudies-arrayexpress