Disease relevance of Eno2

• Regulation of neuron-specific enolase in NG108-15 hybrid cells and C6BU-1 glioma cells [1].
• In rats, NSE increased over 3-fold versus laboratory controls during ischemia of the liver and kidney (both P < 0.0005), but not of the gut [2].
• Therefore, NSE is not a useful early marker of TBI in multiple trauma [2].
• Levels of alpha gamma and gamma gamma forms (nervous system-specific enolases; NSE) in jaundiced rats, which suffer Purkinje cell degeneration due to the inborn hyperbilirubinemia, were three to four times as high as the normal values [3].
• When kernicterus was induced in jaundiced rats by an injection of bucolome, the NSE level in cerebrospinal fluid was elevated up to more than 30-fold the control, together with a significantly higher level of alpha gamma form in blood plasma are helpful in detecting neuronal damage in the central nervous system [3].

Psychiatry related information on Eno2

• Repeated electroconvulsive shock selectively increases the expression of the neuron specific enolase in piriform cortex [4].

High impact information on Eno2

• Thus, NSE and NNE can be used as specific metabolic markers for neurons and glial cells, respectively [5].
• An immunocytochemical study was carried out concerning the distribution of neuron specific enolase in the gastrointestinal tract and pancreas of humans and rats [6].
• The cell lines we report here synthesize neuron-specific enolase, which is a neuron marker, 43-kDa growth-associated protein, a protein associated with neuronal growth cones, and carnosine, a possible olfactory neurotransmitter [7].
• Combined immunohistochemistry for neuron-specific enolase and staining with alcian blue at pH 0.5 was employed on paraffin-embedded sections of normal and Nippostrongylus brasiliensis-infected rat jejunum [8].
• The responsive cells were identified as neurons by their labeling with tetanus toxin and by antibodies to neurofilaments and to the neuron-specific enolase [9].

Chemical compound and disease context of Eno2

• A number of ethylnitrosourea-induced rat tumors were also examined immunohistochemically for NSE: NSE was demonstrated in three anaplastic gliomas; three astrocytomas; and two mixed gliomas [10].
• In SN/CRB co-cultures NSE- and TH-positive cells were more sensitive to glutamate-induced toxicity than in SN/STR co-cultures [11].
• Attenuation of brain injury and reduction of neuron-specific enolase by nicardipine in systemic circulation following focal ischemia and reperfusion in a rat model [12].
• The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death [13].
• Compared with control fetuses, the density of the nerve plexus, ganglia, and number of cell bodies per ganglion immunostained by NSE, VIP, or SP was significantly reduced in OA-TOF fetuses [14].

Biological context of Eno2

• The amino acid sequence deduced from the nucleotide sequence was 433 amino acids in length and showed very high homology (82%) to the amino acid sequence of gamma gamma enolase (neuron-specific enolase: NSE), although the nucleotide sequence showed slightly lower homology (75%) [15].
• These data indicate that gamma-enolase gene expression is associated with the differentiation of the oligodendrocytes and that it is repressed in adult fully mature cells [16].
• The 2,222-nucleotide NSE and mRNA sequence presented identifies a 68-nucleotide 5' noncoding region, a 1,302-nucleotide open reading frame (corresponding to a primary translation product of 434 amino acids), and 852 noncoding 3' bases [17].
• The cDNAs to mRNA for rat gamma gamma enolase (neuron-specific enolase; NSE; EC 4.2.1.11) were isolated from a cDNA library by using differential colony hybridization and a hybrid-selected translation assay [18].
• The NSE-gene spanned about 9 kb and consisted of twelve exons and eleven introns [19].

Anatomical context of Eno2

• During development, both signals coincidentally increased in Purkinje cells and neurons of the dentate nucleus, while only NSE signals showed a gradual increase in the internal granule cells in which NNE signals remained at the same level from early postnatal to adult stages [20].
• Neuron-specific enolase is not only a specific molecular marker for mature nerve cells, but is closely correlated to the differentiated state [21].
• In addition, study of neurons in cerebellum and neocortex reveals that they are NNE(+) during migration and only become NSE(+) in their final location, presumably after making full synaptic connections [21].
• On examination of the adult rat cerebellum, both NSE and NNE signals were detected in all identified and presumed neurons which included Purkinje cells, internal granule cells and presumed stellate/basket cells in the cerebellar cortex and neurons of the dentate nucleus [20].
• Neuron-specific enolase (NSE), and non-neuronal enolase (NNE) which exists in many tissues including liver but is localized in glial cells within the nervous system, were synthesized in the rabbit reticulocyte cell-free translation system programmed with brain mRNAs [22].

Associations of Eno2 with chemical compounds

• Following in vivo destruction of neurons by intracerebral injection of the selective neurotoxin, kainic acid, there was a significant decrease in the activity of NSE and hybrid enolase (neuronal forms) and no change in the activity of NNE (glial form) [23].
• A dose-response relationship was observed between kainate concentration and the amount of NSE released (r = -0.69; p < 0.05) as well as a significant correlation between NSE release and neuronal death (r = 0.64; p < 0.05) [24].
• Identification of neuron-specific enolase and nonneuronal enolase in human and rat brain on two-dimensional polyacrylamide gels [25].
• Neuron-specific enolase and creatine phosphokinase were found, by 2-dimensional gel analysis, in rat brain synaptic plasma membranes (SPM) [26].
• On the other hand, levels of NSE subunit (gamma subunit or 14-3-2 protein) in adipose tissue (0.51 +/- 0.03 gamma gamma-equivalent pmol/mg protein) were increased to 170% of control by serial injection (for 7 days) of epinephrine or norepinephrine with little change of the level of enolase alpha subunit on a mg protein basis [27].

Other interactions of Eno2

• The size of NNE mRNA was approximately 1800 bases by Northern transfer analysis and much shorter than that of NSE mRNA (2400 bases) indicating a short 3'-noncoding region [15].
• These were followed by evaluation of the cortical lesion volume (CLV) after immunostaining for neuron-specific enolase, caspase 3 active, and GFAP [28].
• The ratio between gamma gamma-enolase and alpha gamma-enolase may be indicative of the degree of neuronal maturation, a conclusion further substantiated by the high ratio observed in cerebellum and the low ratio observed in olfactory bulbs, both compared with the ratio in forebrain [29].
• Thus GAP-43 and NSE should be used with caution as neuron-specific markers in studies of normal and pathological neural development [30].
• PRAX-1 mRNA expression was largely neuronal; it colocalized with neuron-specific enolase but not glial fibrillary acidic protein [31].

Analytical, diagnostic and therapeutic context of Eno2

• Neuron-specific enolase (NSE) and non-neuronal enolase (NNE) mRNAs are co-expressed in neurons of the rat cerebellum: in situ hybridization histochemistry [20].
• Molecular cloning and the nucleotide sequence of cDNA for neuron-specific enolase messenger RNA of rat brain [18].
• Primary neuronal cell cultures, derived by centrifugal elutriation of cells dissociated from embryonic rat cerebra, have been analyzed for their content of neuron-specific enolase (NSE) and non-neuronal enolase (NNE) [32].
• Both immunocytochemical staining and radioimmunoassay establish that NSE is present in these cells [32].
• Another method which has been related to neuronal activity is neuron-specific enolase (NSE) immunohistochemistry [33].

References