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Protective Reaction (protective + reaction)
Selected AbstractsInvestigation of Protective Reactions Against Cadmium Toxicity in the Cells Established from a Transgenic Mouse Deficient in the Metallothionein GenesJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 2 2003Tetsuya Abe Objective:, To characterize a fibroblast cell strain which we established from an metallothionein (MT) knock-out (KO) mouse and to determine whether expression of the Hsp genes induced by cadmium is related to expression of the MT-I and -II genes. Methods:, We established a fibroblast cell strain (named "MT-KO2") derived from the peritoneum of an MT-KO mouse which is deficient in the MT-I and -II genes. We determined an expression of MT-I, Hsp32 and Grp 78 genes by Northern blot analysis. Results:, The mRNA level of MT-I, an isoform of the MT gene products, was induced dose-dependently in responce to increasing concentrations of CdCl2 (5,25 µM) in a fibroblast cell strain derived from the peritoneum of an MT wild type mouse (named "MT-W3"). But it was not induced in MT-KO2 cells after the same treatment. There was no significant difference between MT-KO2 and MT-W3 cells in a concentration of intracellular glutathione (reduced form) under normal conditions. MT-KO2 cells were not more sensitive to cytotoxicity of CdCl2 than in MT-W3 cells. Expression of the Hsp32 gene was more extensively enhanced in MT-KO2 cells than in MT-W3 cells after treatment with 5,10 µM CdCl2 for 5 hours. Furthermore, the cellular concentration of reduced glatathione (GSH) was also more increased in MT-KO2 cells than in MT-W3 cells after treatment with 50 µM CdCl2 for 3 hours. Conclusions:, Expression of the Hsp32 gene tends to be increased in MT-KO2 cells in response to cadmium exposure. The expression of the Hsp32 gene and increase in the cellular concentration of GSH may be augmented to compensate for the impaired expression of the MT genes in MT-KO2 cells. [source] N -methyl- d -aspartate, hyperpolarization-activated cation current (Ih) and ,-aminobutyric acid conductances govern the risk of epileptogenesis following febrile seizures in rat hippocampusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2010Mohamed Ouardouz Abstract Febrile seizures are the most common types of seizure in children, and are generally considered to be benign. However, febrile seizures in children with dysgenesis have been associated with the development of temporal lobe epilepsy. We have previously shown in a rat model of dysgenesis (cortical freeze lesion) and hyperthermia-induced seizures that 86% of these animals developed recurrent seizures in adulthood. The cellular changes underlying the increased risk of epileptogenesis in this model are not known. Using whole cell patch-clamp recordings from CA1 hippocampal pyramidal cells, we found a more pronounced increase in excitability in rats with both hyperthermic seizures and dysgenesis than in rats with hyperthermic seizures alone or dysgenesis alone. The change was found to be secondary to an increase in N -methyl- d -aspartate (NMDA) receptor-mediated excitatory postsynaptic currents (EPSCs). Inversely, hyperpolarization-activated cation current was more pronounced in naïve rats with hyperthermic seizures than in rats with dysgenesis and hyperthermic seizures or with dysgenesis alone. The increase in GABAA -mediated inhibition observed was comparable in rats with or without dysgenesis after hyperthermic seizures, whereas no changes were observed in rats with dysgenesis alone. Our work indicates that in this two-hit model, changes in NMDA receptor-mediated EPSCs may facilitate epileptogenesis following febrile seizures. Changes in the hyperpolarization-activated cation currents may represent a protective reaction and act by damping the NMDA receptor-mediated hyperexcitability, rather than converting inhibition into excitation. These findings provide a new hypothesis of cellular changes following hyperthermic seizures in predisposed individuals, and may help in the design of therapeutic strategies to prevent epileptogenesis following prolonged febrile seizures. [source] DnaJB6 is present in the core of Lewy bodies and is highly up-regulated in parkinsonian astrocytesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2009P.F. Durrenberger Abstract DnaJ/Hsp40 chaperones determine the activity of Hsp70s by stabilizing their interaction with substrate proteins. We have predicted, based on the in silico analysis of a brain-derived whole-genome transcriptome data set, an increased expression of DnaJ/Hsp40 homologue, subfamily B, member 6 (DnaJB6) in Parkinson's disease (PD; Moran et al. [2006] Neurogenetics 7:1,11). We now show that DnaJB6 is a novel component of Lewy bodies (LBs) in both PD substantia nigra and PD cortex and that it is strongly up-regulated in parkinsonian astrocytes. The presence of DnaJB6 in the center of LBs suggests an early and direct involvement of this chaperone in the neuronal disease process associated with PD. The strong concomitant expression of DnaJB6 in astrocytes emphasizes the involvement of glial cells in PD and could indicate a route for therapeutic intervention. Extracellular alpha-synuclein originating from intravesicular alpha-synuclein is prone to aggregation and the potential source of extracellular aggregates (Lee [2008] J. Mol. Neurosci. 34:17,22). The observed strong expression of DnaJB6 by astrocytes could reflect a protective reaction, so reducing the neuronal release of toxic alpha-synuclein and supporting the astrocyte response in PD might limit the progression of the disease process. © 2008 Wiley-Liss, Inc. [source] Comment: A biological guide for electromagnetic safety: the stress responseBIOELECTROMAGNETICS, Issue 8 2004Martin Blank Abstract Questions of safety of electromagnetic (EM) fields should be based on relevant biological properties, i.e., specific cellular reactions to potentially harmful stimuli. The stress response is a well documented protective reaction of plant and animal cells to a variety of environmental threats, and it is stimulated by both extremely low frequency (ELF) and radio frequency (RF) EM fields. It involves activation of DNA to initiate synthesis of stress proteins. Thermal and non-thermal stimuli affect different segments of DNA and utilize different biochemical pathways. However, both ELF and RF stimulate the same non-thermal pathway. Since the same biochemical reactions are stimulated in different frequency ranges with very different specific absorption rates (SARs), SAR level is not a valid basis for safety standards. Studies of EM field interactions with DNA and with model systems provide insight into a plausible mechanism that can be effective in ELF and RF ranges. Bioelectromagnetics 25:642,646, 2004. © 2004 Wiley-Liss, Inc. [source] | ||||||||||