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PubMed1998

Can monomers of yeast enolase have enzymatic activity?

Using a combination of ultraviolet spectroscopy under pressure and stopped-flow kinetics under pressure, we have shown that the monomers of yeast enolase produced by hydrostatic pressure are inactive. K(eq), deltaV and deltaV for the dissociation/inactivation produced by hydrostatic pressure have been determined under various conditions. Removing the Mg2+ from enolase, either by adding EDTA or by preparing apoenzyme, displaces the equilibrium towards monomers and decreases both deltaV and deltaV. Loss of Mg2+ contributes to the negative deltaV for dissociation; this loss occurs, at least partially, in the transition state for dissociation. Both removal of Mg(II) and dissociation of the enzyme produce major changes in the intensity of the aromatic region of the CD spectrum. We propose that these changes in the CD spectra reflect changes in the conformations of the 'mobile loops' of enolase. The precise conformation of these, loops is necessary for binding Mg2+ (and, hence, for activity) and for maintaining subunit interactions.

Circular Dichroism↗

PubMed1996

Beta-secretase processing of the beta-amyloid precursor protein in transgenic mice is efficient in neurons but inefficient in astrocytes.

Alzheimer's disease is characterized by the extracellular deposition of beta-amyloid peptide (Abeta) in cerebral plaques and evidence is accumulating that amyloid is neurotoxic. Abeta is derived from the beta-amyloid precursor protein (APP). Proteolytic processing of APP by the enzyme, beta-secretase, produces the N terminus of Abeta, and releases a secreted ectodomain of APP (beta-s-APP). To develop animal models for measuring beta-secretase activity in specific brain cells in vivo, we have targeted the expression of the full-length human APP to either neurons or astrocytes in transgenic mice using the neuron- specific enolase (NSE) promoter or a modified glial fibrillary acidic protein (GFAP) gene, respectively. The APP cDNAs expressed were mutated (KM to NL at 670/671) to encode amino acid substitutions that enhance amyloidogenic processing in vitro. Western analyses revealed abundant production of beta-s-APP in the brains of NSE-APP mice and enzyme-linked immunosorbent assay analyses showed production of Abeta in fetal primary mixed brain cultures and brain homogenates from these transgenic animals. Because the NSE promoter drives expression primarily in neurons, this provides in vivo evidence that the beta-secretase cleavage necessary for generation of beta-s-APP and Abeta is efficiently performed in neurons. In contrast, only little beta-s-APP was detected in brain homogenates of GFAP-APP mice, indicating that astrocytes show very little beta-secretase activity in vivo. This provides strong in vivo evidence that the major source of Abeta in brain is from neurons and not from astrocytes.

Amyloid Precursor Protein Secretases↗

PubMed2001

Brain-specific proteins in the cerebrospinal fluid of severely asphyxiated newborn infants.

UNLABELLED: Upcoming trials of neuroprotective strategies in severely asphyxiated newborn infants emphasize the need for early and objective markers of both good and bad long-term prognosis. Traditional markers such as neurological depression and seizures are not specific. AIM: To study whether measurement in the cerebrospinal fluid of some proteins known to be specific to the central nervous system was in covariance with the clinical course and long-term prognosis. METHODS: Twenty-two asphyxiated infants were included in the study and compared with a control group of 8 infants without signs of perinatal asphyxia. Cerebrospinal fluid (CSF) was collected during the first 4 d of life and analysed for neurofilament protein (NFp), glial fibrillary acidic protein (GFAp), protein S-100 and neuron-specific enolase (NSE). RESULTS: The concentrations of all four proteins were significantly increased in the CSF of asphyxiated infants. The concentrations correlated significantly with other indicators of long-term prognosis and to neurological impairment at I y of age, or death before that time. Specifically, concentrations were excessively high in the five infants who died. CONCLUSIONS: High concentrations of brain-specific proteins are released into the CSF of asphyxiated infants. It might therefore be useful to measure these concentrations when excluding patients with the gravest prognosis from neuroprotective trials.

Asphyxia Neonatorum↗

PubMed2002

Brain damage markers in children. Neurobiological and clinical aspects.

UNLABELLED: The presence in blood of proteins normally confined to the cytoplasm of brain cells is considered peripheral evidence of brain damage. Only recently have these proteins been measured in the blood of children at risk of brain damage. To show the value and limitations of measuring these proteins, we review their biology and the adult literature that has correlated the blood concentrations of these proteins with lesion size and dysfunction. CONCLUSION: We conclude that brain damage markers will increasingly be measured in the blood of newborns and other children at risk of brain damage.

Biomarkers↗

PubMedDate not supplied

Simultaneous expression of glial fibrillary acidic (GFA) protein and neuron-specific enolase (NSE) by the same reactive or neoplastic astrocytes.

In normal cells of the central nervous system (CNS), glial fibrillary acidic (GFA) protein is demonstrable by immunohistochemistry in fibrillated astrocytes, and neuron-specific enolase (NSE) in neurons and their processes. However, it has been shown that NSE may also be expressed in reactive astrocytes and in various neoplastic cells of non-neuronal origin, including those of astrocytomas and glioblastomas. In the present study, a double-labelling technique using immunoperoxidase (PAP) and immunofluorescence (FITC) was employed to determine whether GFA protein and NSE could be expressed simultaneously by the same cell. This was found to be the case in some, but not in all reactive astrocytes in the human brain. In glial tumours, many of the neoplastic cells in the glioblastomas and astrocytomas examined demonstrated either GFA protein or NSE, but usually not both. However, occasional neoplastic cells in those gliomas were found to show both proteins. Because of the relatively low sensitivity of the FITC technique, the percentage of cells expressing both proteins could not be determined, but it is clearly possible for a single reactive or neoplastic astrocyte to demonstrate both GFA protein and NSE.

Antigen-Antibody Reactions↗

PubMed1996

The effects of sodium perchlorate on rabbit muscle enolase--Spectral characterization of the monomer.

Incubation of rabbit beta beta enolase in NaClO4 (< or = O.3 M) results in a loss of enzymatic activity and striking changes in the second-derivative ultraviolet spectrum of enolase. HPLC gel filtration shows that dissociation of the dimeric enzyme is occurring. We have used molecular modelling, fluorescence and circular dichroic spectroscopy to examine the structural differences between the monomeric and dimeric forms of this protein. In the dimer, the tyrosine residues are in a non-polar environment; upon dissociation, two of them that were at the dimer interface become exposed. This results in large changes in the second-derivative spectrum. Both the tryptophan fluorescence emission spectrum and the aromatic region of the CD spectrum indicate that there are also changes in the environment of other aromatic residues. No perturbations in the peptide bond region of the CD spectrum are observed. We propose that the major structural effect of NaClO4 is to increase the flexibility of the loops connecting the helices and strands of the alpha/beta barrel of enolase. These loops, which contain about half of the aromatic residues, contain some of the residues of the active site and other residues involved in subunit contacts. Increased flexibility of the loops could disrupt both subunit interactions and the structure of the active site.

Amino Acids↗

PubMed1995

Brain lesions in calves following transplacental infection with bovine-virus diarrhoea virus.

In 33 calves and subadult cattle of the Holstein-Friesian breed ranging from 1 to 210 days of age, the spectrum of brain lesions induced by intra-uterine infection with bovine-virus diarrhoea virus (BVDV) was retrospectively analysed. Of these, 27 animals originated from herds with a long history of BVD. Six calves were derived from dams vaccinated between the 90th and 118th day of gestation with a BVD live vaccine. The most frequent lesion was cerebellar hypoplasia, being present in 25 out of 33 (76%) of the animals. In most of these cases, cerebellar hypoplasia was associated with hydranencephaly, internal hydrocephalus, microencephaly or porencephaly. In cases with hydranencephaly, the fluid-filled cavities were devoid of ependymal lining. The lumina of the lateral ventricles of these cases were surrounded by glial fibrillary acidic protein (GFAP)-positive cells and a dense layer of immunoreactive cell processes. In the white matter adjacent to the dilated ventricular lumina, a reactive astrocytosis was present. Porencephalic cysts were surrounded by astrocytes with increased expression of GFAP and vimentin-positive cells and cell processes. In hydranencephalic brains, staining for neuron-specific enolase (NSE) revealed a marked reduction of NSE-positive nerve cells in cortical areas. In all six experimental cases and in several field cases with hydranencephaly or internal hydrocephalus, small groups of heterotopic NSE-positive neurons were present in the white matter of the cerebral hemispheres. In markedly hypoplastic cerebella, reduction of the cortical cell layers and degenerative changes in, and heterotopia of, Purkinje cells were found. In these cases, NSE- and neurofilament-positive cell processes were either markedly diminished or only remnants of immunoreactive cell processes were present. In five animals without significant gross cerebellar abnormalities, degenerative changes of Purkinje cells were found. Immunohistochemical staining using antibodies against glial and neuron-specific proteins on these brains, which represent postnatal end-stage lesions of BVDV-induced disturbances of the normal brain development, did not provide any insight into the possible pathogenetic mechanisms of these alterations. Application of immunohistochemistry, however, revealed changes, such as reactive astrocytosis and loss of nerve cell processes, which were not obvious on haematoxylin and eosin (H&E) stained sections.

Animals↗

PubMed1994

An autopsy case of extraskeletal Ewing's sarcoma followed up for 24 years.

A long-term (24 years) follow-up case of extraskeletal Ewing's sarcoma is reported. The light microscopic examination showed features hardly indistinguishable from Ewing's sarcoma of the bone, that is, the tumor cells were diffusely arranged and uniform in size and shape, and possessed glycogen in the cytoplasm. Homer-Wright rosettes were found only in the autopsy material. An immunohistochemical study using a neural marker (neuron-specific enolase) demonstrated positive staining in most tumor cells. An ultrastructural study revealed intracytoplasmic glycogen particles and incomplete neural characters as follows: the cytoplasmic processes resembled neural processes without neurosecretory granules, microtubules or neurofilaments. These findings suggest that this case finally acquired an incomplete neural character with repeated recurrence. This tumor was diagnosed extraskeletal Ewing's sarcoma, but in future it may be categorized as primitive neuroectodermal tumor (PNET).

Adult↗

PubMed2006

Chronic treatment with high doses of corticosterone decreases cytoskeletal proteins in the rat hippocampus.

Hypercortisolism is a common trait of Cushing's disease and depression. These two disorders also share hippocampal volume decrease and cognitive deficits. However, experimentally induced hypercortisolism induces neuronal atrophy, which has been proposed to be the phenomenon underlying the hippocampal shrinkage. We hypothesized that the above-mentioned atrophy is due to a deleterious effect of high concentrations of glucocorticoids on cytoskeletal proteins. One or two pellets (100 mg each) of corticosterone were subcutaneously implanted in adult rats. Twenty-one days later, light, medium and heavy subunits of intermediate neurofilaments (NFL, NFM and NFH) and the microtubule-associated protein 2 (MAP2) were quantified by immunohistochemistry in Ammon's horn and dentate gyrus. We also evaluated the in vitro glutamate release in hippocampal slices. Both doses of corticosterone induced a decrement of NFL, NFM and NFH in both hippocampal areas but only 200 mg decreased MAP2. This dose also diminished the potassium-stimulated glutamate release. All of these changes seemed not to be due to neuron loss, as no decrement in neuron-specific nuclear protein-positive cells was found. With the exception of NFL, the above-mentioned diminution was not observed in the globus pallidus, one of the brain regions with the lowest glucocorticoid receptor density. These results provide a subcellular insight into the trophic changes found in experimental models of hypercortisolism. The coincidence between decrements in MAP2 and glutamate release suggests possible links between high glucocorticoid levels, dendritic atrophy and the cognitive impairment reported in patients suffering from Cushing's disease and depression.

Animals↗

PubMed2006

Differential effects of haloperidol and olanzapine on the expression of erythropoietin and its receptor in rat hippocampus and striatum.

Compared with first-generation antipsychotics (FGAs), second-generation antipsychotics (SGAs) seem to be neuroprotective and trigger neuroplasticity. Because neuroplasticity is regulated by a variety of neurotrophic factors we studied differential effects of haloperidol (HAL, a FGA) and olanzapine (OLZ, a SGA) on temporal expression of erythropoietin (EPO), a potent neuroprotective factor and its receptor (EPOr) in rat brain. Rats (8-10/group) were treated with HAL or OLZ for 14 days (HAL-14 or OLZ-14) or 45 days (HAL-45 or OLZ-45). Animals were killed by decapitation or by perfusion to collect brains for immunoblotting and immunohistochemical analysis respectively. In hippocampus, the levels of both EPO and EPOr were significantly increased in HAL-14 (p < 0.001) and OLZ-14 (p < 0.001) groups. Their levels decreased in HAL-45 compared with levels in HAL-14 (EPO, p < 0.001; EPOr, p < 0.05), whereas the levels were further increased (EPO, p < 0.05) in OLZ-45 compared with OLZ-14. In striatum, the levels of both EPO and EPOr were unchanged in HAL-14 and EPO levels significantly decreased in HAL-45 (p < 0.05), whereas their levels were significantly increased in OLZ-14 and OLZ-45 compared with the vehicle-treated control (p < 0.001). Both EPO and EPOr were primarily expressed by neurons and endothelial cells. These data suggest that SGAs such as OLZ may have neuroprotective effects through expression of EPO that may be clinically relevant for long-term safe and beneficial management of psychotic patients.

Animals↗

PubMed2000

Tumor markers in neuroendocrine tumors.

Most neuroendocrine tumors produce and secrete a multitude of peptide hormones and amines. Some of these substances cause a specific clinical syndrome: carcinoid, Zollinger-Ellison, hyperglycemic, glucagonoma and WDHA syndrome. Specific markers for these syndromes are basal and/or stimulated levels of urinary 5-HIAA, serum or plasma gastrin, insulin, glucagon and vasoactive intestinal polypeptide, respectively. Some carcinoid tumors and about one third of endocrine pancreatic tumors do not present any clinical symptoms and are called 'nonfunctioning' tumors. Therefore, general tumor markers such as chromogranin A, pancreatic polypeptide, serum neuron-specific enolase and subunits of glycoprotein hormones have been used for screening purposes in patients without distinct clinical hormone-related symptoms. Among these general tumor markers chromogranin A, although its precise function is not yet established, has been shown to be a very sensitive and specific serum marker for various types of neuroendocrine tumors. This is because it may also be elevated in many cases of less well-differentiated tumors of neuroendocrine origin that do not secrete known hormones. At the moment, chromogranin A is considered the best general neuroendocrine serum or plasma marker available both for diagnosis and therapeutic evaluation and is increased in 50-100% of patients with various neuroendocrine tumors. Chromogranin A serum or plasma levels reflect tumor load, and it may be an independent marker of prognosis in patients with midgut carcinoids.

Biomarkers, Tumor↗

PubMedDate not supplied

Developmental neurotoxicity of toluene: in vivo and in vitro effects on astroglial cells.

Toluene, an inexpensive and available industrial solvent, has become increasingly popular as a drug of abuse. Inhaling toluene leads to a feeling of euphoria and several reports have shown that children born to women who had abused toluene during pregnancy present a syndrome (toluene embryopathy or fetal solvent syndrome) that is characterized by CNS effects (e.g. microencephaly), growth retardation and facial dysmorphologies. The characteristics of the fetal solvent syndrome are very similar to those observed in the fetal alcohol syndrome. As exposure of rats to ethanol during the brain growth spurt has been shown to cause microencephaly and to affect glial cell proliferation and maturation, the present study examines the effects of toluene administration (250, 500 and 750 mg/kg) in neonatal rats from postnatal day 4 to 10. This treatment resulted in a significant decrease in both brain and body weights, and in a significant reduction of levels of glial fibrillary acidic protein, but not of neuron-specific enolase in rat brain. In vitro experiments demonstrate that pharmacologically relevant concentrations of toluene (250-1,000 microM) significantly inhibit proliferation of rat cortical astrocytes without causing overt cytotoxicity. These results indicate that toluene does not cause selective microencephaly; however, it affects brain weight, and appears to target developing astrocytes, possibly by inhibiting their proliferation.

Aging↗

PubMedDate not supplied

Enolases are highly conserved fungal allergens.

BACKGROUND: Lack of knowledge of the identity of fungal allergens still is a major obstacle for improvement of diagnosis and therapy of allergies to moulds. We have therefore further analyzed the allergens of the two moulds, Alternaria alternata and Cladosporium herbarum and found that enolases (EC 4.2.1.11) are major allergens, at least of the two fungal species just mentioned. METHODS: The enolases of Alternaria and Cladosporium were cloned from cDNA libraries constructed from vegetative cells of the two moulds by immunological screening with sera from selected patients allergic to the moulds. The two enolases were expressed as recombinant nonfusion proteins and used for determination of the incidence of allergy to enolase among a cohort of patients. RESULTS: Sequencing of the two enolases showed very close relationships with other known fungal enolase sequences. Competition experiments using immunoblots of the recombinant nonfusion proteins showed nearly complete identity of the epitopes on both enolases. Serum from a patient reactive to Cladosporium enolase reacted equally well with the enolases of Alternaria, Saccharomyces and Candida. About 50% each of the sera from patients reactive to Cladosporium and Alternaria were strongly reactive to the recombinant enolases. CONCLUSIONS: Enolases are therefore considered to be highly conserved major fungal allergens.

Allergens↗

PubMed1997

Rhabdoid tumor in the brain of a dog.

Rhabdoid tumor is a neoplasm of uncertain cellular origin recognized in humans. These tumors most commonly arise in the kidneys of children, but they can also affect many extrarenal sites, including the central nervous system. Similar neoplasms have not been reported in nonprimate species. A malignant brain tumor in a young dog was characterized by large cells with globular intracytoplasmic inclusions composed of intermediate filaments. By immunohistochemistry, neoplastic cells were uniformly reactive for vimentin and demonstrated scattered reactivity for glial fibrillary acidic protein and neuron-specific enolase. The intermediate filaments also reacted with vimentin antibodies by immunogold electron microscopy. The findings in this case are remarkably similar to the histologic, ultrastructural, and immunocytochemical features of rhabdoid tumors in humans.

Animals↗

PubMed2002

Immunohistochemical staining patterns of canine meningiomas and correlation with published immunophenotypes.

This study examined immunohistochemical staining patterns for several meningioma variants involving either the brain or spinal cord of dogs. Formalin-fixed, paraffin-embedded tissue from 15 tumors was obtained. The selected tumor group included seven meningothelial, three transitional, two malignant (anaplastic), one myxoid, one papillary, and one osteomatous meningiomas. Tumors were evaluated for reactivity to the following six immunohistochemical markers: vimentin, pancytokeratin, glial fibrillary acidic protein (GFAP), S100, neuron-specific enolase (NSE), and synaptophysin. Vimentin expression was detected in all meningiomas, and 14 of 15 tumors demonstrated intense vimentin staining in more than 50% of the neoplastic cells. Pancytokeratin expression was present in 11 of 15 neoplasms; however, positive staining frequently was focal and often involved a small percentage of the neoplastic cells. GFAP expression was detected in a single, anaplastic meningioma. Although expression of NSE and S100 was detected in 12 of 25 meningiomas, the intensity of the staining and the percentage of positive neoplastic cells was highly variable. Synaptophysin was uniformly negative. These results will help to establish immunohistochemical profiles for meningiomas that will improve our ability to correctly differentiate these neoplasms of meningeal origin from central nervous system tumors originating from other sites.

Animals↗

PubMed1996

Glutamate-induced efflux of protein, neuron-specific enolase and lactate dehydrogenase from a mesencephalic cell culture.

A mixed mesencephalic cell culture damaged by glutamate was used as a model to study the efflux of lactate dehydrogenase and neuron-specific enolase from neuronal cells into the culture medium. Glutamate toxicity was induced in sister cultures by 15 min exposure to 100 mumol/l glutamate in a Ca2+ containing salt solution. Cell injury was monitored 24 h later by measuring the lactate dehydrogenase activity and the neuron-specific enolase content in the cells and in the culture medium. The neuronal cell damage is reflected by an efflux of neuron-specific enolase and lactate dehydrogenase from the cells and an increase of lactate dehydrogenase catalytic activity concentration and neuron-specific enolase mass concentration in the culture medium. It was found that the efflux fraction calculated from estimations of the cells was clearly higher than the efflux fraction calculated from estimations of the amount of enzymes found in the culture medium. Calculations of the recovery of lactate dehydrogenase and neuron-specific enolase and experiments designed to study the efflux of lactate dehydrogenase and neuron-specific enolase during incubation and washing showed that higher amounts of neuron-specific enolase are released than lactate dehydrogenase. A close correlation was found between the glutamate-induced changes of the neuron-specific enolase efflux fraction, based on enzyme determinations of the cells, and the change of the microscopically counted neuron-specific enolase immunoreactive cell numbers. This indicates that the determination of the neuron-specific enolase efflux fraction (cells) is an accurate and sensitive marker of damaged neurons. The lactate dehydrogenase efflux fraction seems to be less sensitive for the quantitation of neuronal cell damage; in addition, it depends not only on the neuronal damage but also on the proportion of neurons in the cell culture.

Animals↗

PubMed1996

Plasma levels of chromogranin A are directly proportional to tumour burden in neuroblastoma.

A novel animal experimental model involving the human, poorly differentiated, and adrenergic neuroblastoma cell line SH-SY5Y xenotransplanted to subcutaneous tissue of 13 nude rats (WAG rnu/rnu) was used to investigate the usefulness of six proposed neuroblastoma markers. It was shown that the plasma concentrations of human chromogranin A (CgA) as measured by RIA were directly proportional to tumour volume (r = 0.83, P < 0.001). To rule out possible liberation of CgA by tumour cell lysis, the CgA degradation product pancreastatin was also measured in plasma by a specific RIA, but was not detectable. Plasma neurone-specific enolase (NSE) was elevated in tumour-bearing animals (P < 0.01), but did not correlate with tumour volume (r = 0.49, P > 0.05). Urine homovanillic acid (HVA), detected by HPLC, was elevated in tumour-bearing animals (P < 0.01), but did not correlate with tumour volume (r = -0.32, P > 0.05). Urine vanillyl mandelic acid was not detectable. Urine dopamine was found in low concentrations that did not correlate with tumour volume. In summary, although plasma NSE and urinary HVA were elevated in tumour-bearing animals only plasma CgA correlated with tumour burden. This makes CgA a promising biochemical marker for neuroblastomas.

Adrenal Gland Neoplasms↗

PubMed2004

Neuroendocrine tumor markers and enterochromaffin-like cell hyper/dysplasia in type 1 diabetes.

OBJECTIVE: Parietal cell antibodies (PCAs) are found in 20% of type 1 diabetic patients, denoting autoimmune gastritis and pernicious anemia, which may predispose to enterochromaffin-like (ECL) cell hyper/dysplasia and gastric carcinoid tumors. We evaluated whether chromogranin A (CgA), 5-hydroxyindole acetic acid (5-HIAA), and neuron-specific enolase (NSE) contribute to screening for ECL cell hyper/dysplasia. RESEARCH DESIGN AND METHODS: Sera from 93 type 1 diabetic patients (53 men and 40 women, 31 PCA(+) and 62 PCA(-), aged 45 +/- 13 years) were analyzed for PCAs by indirect immunofluorescence and for CgA, NSE, and gastrin by radioimmunoassay. Urinary 5-HIAA was tested by high-performance liquid chromatography. Corpus atrophy and ECL cell proliferation were assessed in gastric biopsies. RESULTS: PCA(+) patients had higher gastrin (P < 0.0001) and CgA levels (P = 0.003) and were more prone to autoimmune gastritis (odds ratio [OR] 17, P < 0.0001) and ECL cell hyper/dysplasia (OR = 23, P = 0.005) than PCA(-) subjects. ECL cell hyper/dysplasia was present in seven PCA(+) patients who showed higher CgA levels (P < 0.0001) than subjects without ECL cell hyper/dysplasia, but NSE and 5-HIAA levels were similar. CgA levels correlated with gastrinemia (r = 0.50, P < 0.0001), PCA titer (r = 0.42, P = 0.001), and 5-HIAA levels (r = 0.38, P = 0.012). Logistic regression identified the CgA level (beta = 0.01, P = 0.027) as an independent risk factor for ECL cell hyper/dysplasia when PCA, CgA, 5-HIAA, NSE, gastrin, sex, and age were tested. Multivariate linear regression demonstrated that CgA level was determined by ECL cell density (r = 0.59, P < 0.0001) and gastrin level (r = 0.67, P = 0.02). One PCA(+) patient with elevated gastrin, CgA, and 5-HIAA levels had a gastric carcinoid tumor. CONCLUSIONS: PCA(+) patients, particularly those with high gastrin and CgA levels, risk developing ECL cell hyper/dysplasia. The determination of CgA, but not NSE and 5-HIAA, may complement histology in evaluating ECL cell mass.

Autoantibodies↗