scholarly journals Electrochemically Reduced Water Protects Neural Cells from Oxidative Damage

2014 ◽  
Vol 2014 ◽  
pp. 1-18 ◽  
Author(s):  
Taichi Kashiwagi ◽  
Hanxu Yan ◽  
Takeki Hamasaki ◽  
Tomoya Kinjo ◽  
Noboru Nakamichi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Neuronal Cell ◽  
Cell Types ◽  
Aging Brain ◽  
Neural Cells ◽  
Primary Cells ◽  
Oxidative Stresses ◽  
Rate Of Oxygen Consumption ◽  
Neuronal Cell Lines ◽  
Reduced Water

Aging-related neurodegenerative disorders are closely associated with mitochondrial dysfunction and oxidative stresses and their incidence tends to increase with aging. Brain is the most vulnerable to reactive species generated by a higher rate of oxygen consumption and glucose utilization compared to other organs. Electrochemically reduced water (ERW) was demonstrated to scavenge reactive oxygen species (ROS) in several cell types. In the present study, the protective effect of ERW against hydrogen peroxide (H2O2) and nitric oxide (NO) was investigated in several rodent neuronal cell lines and primary cells. ERW was found to significantly suppress H2O2(50–200 μM) induced PC12 and SFME cell deaths. ERW scavenged intracellular ROS and exhibited a protective effect against neuronal network damage caused by 200 μM H2O2in N1E-115 cells. ERW significantly suppressed NO-induced cytotoxicity in PC12 cells despite the fact that it did not have the ability to scavenge intracellular NO. ERW significantly suppressed both glutamate induced Ca2+influx and the resulting cytotoxicity in primary cells. These results collectively demonstrated for the first time that ERW protects several types of neuronal cells by scavenging ROS because of the presence of hydrogen and platinum nanoparticles dissolved in ERW.

scholarly journals A prokaryotic viral sequence is expressed and conserved in mammalian brain

2017 ◽  
Vol 114 (27) ◽  
pp. 7118-7123 ◽  
Author(s):  
Yang-Hui Yeh ◽  
Vignesh Gunasekharan ◽  
Laura Manuelidis
Keyword(s):  
Maternal Inheritance ◽  
Neuronal Cell ◽  
Proteinase K ◽  
Mammalian Brain ◽  
Neural Cells ◽  
Mammalian Evolution ◽  
Western Blots ◽  
Neuronal Cell Lines ◽  
Viral Sequences ◽  
The Brain

A natural and permanent transfer of prokaryotic viral sequences to mammals has not been reported by others. Circular “SPHINX” DNAs <5 kb were previously isolated from nuclease-protected cytoplasmic particles in rodent neuronal cell lines and brain. Two of these DNAs were sequenced after Φ29 polymerase amplification, and they revealed significant but imperfect homology to segments of commensalAcinetobacterphage viruses. These findings were surprising because the brain is isolated from environmental microorganisms. The 1.76-kb DNA sequence (SPHINX 1.8), with an iteron before its ORF, was evaluated here for its expression in neural cells and brain. A rabbit affinity purified antibody generated against a peptide without homology to mammalian sequences labeled a nonglycosylated ∼41-kDa protein (spx1) on Western blots, and the signal was efficiently blocked by the competing peptide. Spx1 was resistant to limited proteinase K digestion, but was unrelated to the expression of host prion protein or its pathologic amyloid form. Remarkably, spx1 concentrated in selected brain synapses, such as those on anterior motor horn neurons that integrate many complex neural inputs. SPHINX 1.8 appears to be involved in tissue-specific differentiation, including essential functions that preserve its propagation during mammalian evolution, possibly via maternal inheritance. The data here indicate that mammals can share and exchange a larger world of prokaryotic viruses than previously envisioned.

scholarly journals Profiling of Sexually Dimorphic Genes in Neural Cells to Identify Eif2s3y, Whose Overexpression Causes Autism-Like Behaviors in Male Mice

2021 ◽  
Vol 9 ◽  
Author(s):  
Muxian Zhang ◽  
Yunqiang Zhou ◽  
Yiru Jiang ◽  
Zhancheng Lu ◽  
Xiaoxia Xiao ◽  
...  
Keyword(s):  
Sex Differences ◽  
Y Chromosome ◽  
Neurological Disorders ◽  
Cell Types ◽  
Neural Cells ◽  
Sexually Dimorphic ◽  
Primary Neurons ◽  
Primary Cells ◽  
Male Mice ◽  
Cellular Mechanisms

Many neurological disorders exhibit sex differences and sex-specific therapeutic responses. Unfortunately, significant amounts of studies investigating molecular and cellular mechanisms underlying these neurological disorders use primary cell cultures with undetermined sexes; and this may be a source for contradictory results among different studies and impair the validity of study conclusion. Herein, we comprehensively compared sexual dimorphism of gene expression in primary neurons, astrocytes, and microglia derived from neonatal mouse brains. We found that overall sexually dimorphic gene numbers were relatively low in these primary cells, with microglia possessing the most (264 genes), neurons possessing the medium (69 genes), and astrocytes possessing the least (30 genes). KEGG analysis indicated that sexually dimorphic genes in these three cell types were strongly enriched for the immune system and immune-related diseases. Furthermore, we identified that sexually dimorphic genes shared by these primary cells dominantly located on the Y chromosome, including Ddx3y, Eif2s3y, Kdm5d, and Uty. Finally, we demonstrated that overexpression of Eif2s3y increased synaptic transmission specifically in male neurons and caused autism-like behaviors specifically in male mice. Together, our results demonstrate that the sex of primary cells should be considered when these cells are used for studying the molecular mechanism underlying neurological disorders with sex-biased susceptibility, especially those related to immune dysfunction. Moreover, our findings indicate that dysregulation of sexually dimorphic genes on the Y chromosome may also result in autism and possibly other neurological disorders, providing new insights into the genetic driver of sex differences in neurological disorders.

scholarly journals Neuromesodermal progenitor origin of trunk neural crest in vivo

2021 ◽  
Author(s):  
Martyna Lukoseviciute ◽  
Sarah Mayes ◽  
Tatjana Sauka-Spengler
Keyword(s):  
Neural Crest ◽  
Single Cell Analysis ◽  
Neuronal Cell ◽  
Cell Types ◽  
Neural Cells ◽  
Embryonic Cells ◽  
Cell Fates ◽  
Trunk Neural Crest ◽  
Bona Fide

AbstractNeural crest (NC) is a vertebrate-specific population of multipotent embryonic cells predisposed to particular derivatives along the anteroposterior (A-P) axis. While only cranial NC progenitors give rise to ectomesenchymal cell types, trunk NC is biased for neuronal cell fates. By integrating multimodal single-cell analysis we uncovered heterogenous NC cells across the entire A-P axis expressing NC regulator foxd3. We pinpointed to its specific cranial and trunk auto-regulated enhancers. The trunk foxd3 enhancer, however, did not mark the bona fide NC, but bipotent tailbud neuromesodermal progenitors (NMps). A subset of these NMp-derived pro-neural cells appeared to give rise to neuronal trunk NC in amniotes in vivo, suggesting that at least a portion of trunk NC progenitors with a bias for neuronal fates originated from NMps in vivo.

scholarly journals Generation of a Phenotypic Array of Hypothalamic Neuronal Cell Models to Study Complex Neuroendocrine Disorders

Endocrinology ◽  
2004 ◽  
Vol 145 (1) ◽  
pp. 393-400 ◽  
Author(s):  
Denise D. Belsham ◽  
Fang Cai ◽  
Hong Cui ◽  
Simon R. Smukler ◽  
Anne Marie F. Salapatek ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Cell Lines ◽  
Neuronal Cell ◽  
Cell Types ◽  
Hormonal Control ◽  
Therapeutic Interventions ◽  
Cell Models ◽  
Virtual Absence ◽  
Neuronal Cell Lines ◽  
Hypothalamic Cells

Abstract Knowledge of how the brain achieves its diverse central control of basic physiology is severely limited by the virtual absence of appropriate cell models. Isolation of clonal populations of unique peptidergic neurons from the hypothalamus will facilitate these studies. Herein we describe the mass immortalization of mouse primary hypothalamic cells in monolayer culture, resulting in the generation of a vast representation of hypothalamic cell types. Subcloning of the heterogeneous cell populations resulted in the establishment of 38 representative clonal neuronal cell lines, of which 16 have been further characterized by analysis of 28 neuroendocrine markers. These cell lines represent the first available models to study the regulation of neuropeptides associated with the control of feeding behavior, including neuropeptide Y, ghrelin, urocortin, proopiomelanocortin, melanin-concentrating hormone, neurotensin, proglucagon, and GHRH. Importantly, a representative cell line responds appropriately to leptin stimulation and results in the repression of neuropeptide Y gene expression. These cell models can be used for detailed molecular analysis of neuropeptide gene regulation and signal transduction events involved in the direct hormonal control of unique hypothalamic neurons, not yet possible in the whole brain. Such studies may contribute information necessary for the strategic design of therapeutic interventions for complex neuroendocrine disorders, such as obesity.

scholarly journals Individual neural cell types express immunologically distinct N-CAM forms.

1985 ◽  
Vol 101 (1) ◽  
pp. 36-42 ◽  
Author(s):  
R K Williams ◽  
C Goridis ◽  
R Akeson
Keyword(s):  
Cell Lines ◽  
Primary Cultures ◽  
Neuronal Cell ◽  
Cell Types ◽  
Neural Cell ◽  
Adult Brain ◽  
Molecular Weights ◽  
Adult Rat ◽  
Cerebellar Neuron ◽  
Neuronal Cell Lines

The neural cell adhesion molecules, or N-CAMs, are a group of structurally and immunologically related glycoproteins found in vertebrate neural tissues. Adult brain N-CAMs have apparent molecular weights of 180,000, 140,000, and 120,000. In this article we identify, using monoclonal antibody (Mab) 3G6.41, an immunologically distinct adult rat N-CAM form and show that this form is selectively expressed by some clonal neural cell lines. Consecutive immunoprecipitation experiments indicate that rabbit anti-N-CAM can remove from solubilized cerebellar neuron primary cultures all 180,000- and 140,000-mol-wt N-CAM molecules that react with Mab 3G6.41. However Mab 3G6.41 cannot remove all N-CAM molecules that react with rabbit anti-N-CAM. Rabbit anti-N-CAM binds to and immunoprecipitates N-CAM forms from the rat neuronal cell lines B35, B65, and B104, the glial lines B12 and C6, and L6 myoblasts. Mab 3G6.41 does not bind to or immunoprecipitate N-CAM from the B12 and B65 lines but does react with the other four lines by both criteria. Many cells in primary cultures of postnatal rat that express glial fibrillary acidic protein also bind Mab 3G6.41. Thus a unique form of rat N-CAM recognized by Mab 3G6.41 is found on some but not all neuronal, glial, and muscle cells.

scholarly journals Chromosome Instability, Aging and Brain Diseases

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1256
Author(s):  
Ivan Y. Iourov ◽  
Yuri B. Yurov ◽  
Svetlana G. Vorsanova ◽  
Sergei I. Kutsev
Keyword(s):  
Brain Aging ◽  
Chromosome Instability ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Accelerated Aging ◽  
Brain Diseases ◽  
Aging Brain ◽  
Ontogenetic Changes ◽  
Health And Disease

Chromosome instability (CIN) has been repeatedly associated with aging and progeroid phenotypes. Moreover, brain-specific CIN seems to be an important element of pathogenic cascades leading to neurodegeneration in late adulthood. Alternatively, CIN and aneuploidy (chromosomal loss/gain) syndromes exhibit accelerated aging phenotypes. Molecularly, cellular senescence, which seems to be mediated by CIN and aneuploidy, is likely to contribute to brain aging in health and disease. However, there is no consensus about the occurrence of CIN in the aging brain. As a result, the role of CIN/somatic aneuploidy in normal and pathological brain aging is a matter of debate. Still, taking into account the effects of CIN on cellular homeostasis, the possibility of involvement in brain aging is highly likely. More importantly, the CIN contribution to neuronal cell death may be responsible for neurodegeneration and the aging-related deterioration of the brain. The loss of CIN-affected neurons probably underlies the contradiction between reports addressing ontogenetic changes of karyotypes within the aged brain. In future studies, the combination of single-cell visualization and whole-genome techniques with systems biology methods would certainly define the intrinsic role of CIN in the aging of the normal and diseased brain.

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