Disease relevance of Eno1

• Enolase isozymes in differentiated and undifferentiated medullary thyroid carcinomas [1].
• Enzyme immunoassay of the serum neurospecific antigens (gliofibrillar acid protein and neurospecific enolase) was used for evaluation of the resistance of the blood-brain barrier in Wistar rats with perinatal hypoxia and ischemia of the CNS [2].
• Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia [3].
• In controls serum levels of gliofibrillar acid protein and neurospecific enolase virtually did not change during postnatal development, while in animals with cerebral hypoxia and ischemia induced in fetuses by both methods serum concentration of neurospecific enolase sharply increased 1 week after the injury and increased on weeks 6 and 10 [2].
• The etiology of toxic peripheral neuropathies: in vitro effects of acrylamide and 2,5-hexanedione on brain enolase and other glycolytic enzymes [4].

High impact information on Eno1

• Thus, NSE and NNE can be used as specific metabolic markers for neurons and glial cells, respectively [5].
• The NNE is located in glial cells with no staining of endothelial cells or neurons [5].
• We immunoprecipitated pp60c-src from Ang II-stimulated vascular smooth muscle cells and measured pp60c-src activity by autophosphorylation and by phosphorylation of enolase [6].
• In this report, we demonstrate that whereas C-SRC expression is not required for expression of HIF-1 or transcriptional activation of genes encoding VEGF and enolase 1 (ENO1), cells expressing the v-Src oncogene have increased expression of HIF-1, VEGF, and ENO1 under both hypoxic and nonhypoxic conditions [7].
• Additionally, relatively larger amounts of 2 metabolic enzymes, creatine phosphokinase and nerve-specific enolase, were present in SCb in ON axons than in DRG or VMN axons [8].

Biological context of Eno1

• Molecular cloning and the nucleotide sequence of cDNA to mRNA for non-neuronal enolase (alpha alpha enolase) of rat brain and liver [9].
• By contrast, no significant change in alpha-enolase gene expression was observed [10].
• Amino acid sequence analysis of polypeptides derived from the cleavage of the protein with cyanogen bromide and V8 protease revealed that the 45-kDa protein is identical to rat alpha-enolase [11].
• During muscle development, an isozymic transition of the glycolytic enzyme enolase occurs from the embryonic and ubiquitous alphaalpha-isoform to the muscle-specific betabeta-isoform [12].
• There is evidence that the gene for gamma-gamma enolase (neuron specific enolase, NSE) is regulated during cell differentiation and development, conserved in a variety of organisms and contains mRNA destabilizing sequences [13].

Anatomical context of Eno1

• High NSE (gamma gamma and alpha gamma) enolase activity was detected in cultured oligodendrocytes [10].
• Thus, nerve cells must undergo a switch from NNE to NSE [14].
• 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 [15].
• 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 [16].
• The purpose of this study was to follow any changes in NSE and/or NNE in cranial motor neurons after separation of their cell bodies from their axon terminals [17].

Associations of Eno1 with chemical compounds

• Three forms of the glycolytic enzyme, enolase [2-phospho-D-glycerate hydrolase (E.C. No. 4.2.1.11)] have been prepared from rat whole brain extract [18].
• 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) [19].
• Identification of neuron-specific enolase and nonneuronal enolase in human and rat brain on two-dimensional polyacrylamide gels [20].
• Neurone-specific enolase and creatine phosphokinase are protein components of rat brain synaptic plasma membranes [21].
• The specific enzymatic activities of enolase and creatine phosphokinase, as well as of pyruvate kinase, also present on the membranes, were comparable to those in the homogenates when these three enzymes were fully activated [21].

Physical interactions of Eno1

• Plasminogen binds specifically to alpha-enolase on rat neuronal plasma membrane [11].

Regulatory relationships of Eno1

• 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 [22].
• ERK1/2 regulates intracellular ATP levels through alpha-enolase expression in cardiomyocytes exposed to ischemic hypoxia and reoxygenation [23].

Other interactions of Eno1

• 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 [9].
• Treatment with basic fibroblast growth factor, which stimulates the proliferation of oligodendrocyte precursor cells and reversibly blocks their differentiation, resulted in lower alpha gamma- and gamma gamma-enolase activities in these cells, but it enhanced alpha alpha-enolase activity slightly [10].
• In fetal and neonatal hearts, muscle-specific beta-enolase gene expression is a minor contributor to total enolase [24].
• However, at 39 degrees C, the cells produced dendritic, neuronal-like processes and elevated levels of NF68 and MAP2, as well as the neuronal markers synaptophysin, neurone-specific enolase, and low levels of tau, all determined by western blotting and immunofluorescent staining [25].
• Enzymatic markers of nerve cell development were measured (enolase isoenzymes and glutamine synthetase) [26].

Analytical, diagnostic and therapeutic context of Eno1

• Neuron-specific enolase (NSE) and non-neuronal enolase (NNE) mRNAs are co-expressed in neurons of the rat cerebellum: in situ hybridization histochemistry [15].
• Immunocytochemical localization and developmental profile of neuron specific enolase (NSE) and non-neuronal enolase (NNE) in aggregating cell cultures of fetal rat brain [27].
• The results indicated excellent agreement between this enzymatically determined ratio and published values of a similar ratio (NNE/NSE) determined by radioimmunoassay for enzyme protein [19].
• Contents of the three forms (alpha alpha, alpha gamma, and gamma gamma) of enolase isozymes and S-100 protein in superior cervical sympathetic ganglia (SCG) excised from rats were determined by the sensitive method of enzyme immunoassay, after application of various forms of stimulation, during incubation for 3 h at 37 degrees C in vitro [28].
• Among enolase isozymes in the SCG, neuron-specific gamma gamma-enolase decreased rapidly after denervation and stayed at a low level for 2 weeks, whereas the isozyme remained almost unchanged after axotomy [29].

References