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PubMed2000

Nerve tissue protein S-100 and neurone-specific enolase concentrations in cerebrospinal fluid and blood during carotid endarterectomy.

Nerve tissue protein S-100 and neurone-specific enolase levels in serum were studied in 10 patients before, during and for 2 days after elective carotid endarterectomy performed under general anaesthesia and using a Javid Shunt. In six patients, simultaneous cerebrospinal fluid samples were also obtained. Serum nerve tissue protein S-100 was normal throughout the operation, but in one patient with severe hypertension, levels increased to 1.38 microg. l-1 at 1 h postoperatively. Two patients showed an increase in cerebrospinal fluid nerve tissue protein S-100 during clamping: these patients also had neurological deficits at 6 months. Serum neurone-specific enolase increased from 5.8 to 9.3 microg.l-1 during shunting while cerebrospinal fluid neurone-specific enolase did not change. Uncomplicated carotid endarterectomy does not produce cerebral damage as measured by serum nerve tissue protein S-100; cerebrospinal fluid nerve tissue protein S-100 may be more sensitive for minor cerebral damage. Neurone-specific enolase appeared to be nonspecific. The lack of correlation between the neuroproteins may need to be explained before relying on these simple assays as diagnostic indicators of cerebral ischaemia.

Aged↗

PubMed1983

Severe head trauma and the changes of concentration of neuron-specific enolase in plasma and in cerebrospinal fluid.

In nine patients with severe head trauma, the concentration of neuron-specific enolase in cerebrospinal fluid and in plasma was determined and compared with the activity of creatine kinase and alpha-hydroxybutyrate dehydrogenase, and with the concentration of lactate. In patients who died of the head trauma, a concentration of neuron-specific enolase of 6.8-64 micrograms/l in the plasma (reference range: 3.0-6.0 micrograms/l) and of 2.2-9.0 micrograms/l in the cerebrospinal fluid (reference range: 0.5-2.0 micrograms/l) was detected. Investigations of three patients showed that the changes of the concentration of neuron-specific enolase in plasma and in cerebrospinal fluid were independent of each other. Furthermore, the initial concentration of neuron-specific enolase in the plasma after the accident and the dynamics of its changes during the disease show a close relationship to the outcome.

Adult↗

PubMed1988

Neurone specific enolase in amniotic fluid: a potential marker of anencephaly.

Normal values for neurone specific enolase in amniotic fluid have been found to follow a non gaussian distribution with a 1-99 centile range of 1.10-4.32 micrograms/L. Neurone specific enolase levels have been shown to be raised in the amniotic fluid of pregnancies complicated by anencephaly, although not those complicated by open spina bifida. Neurone specific enolase measured by radioimmunoassay is capable of totally discriminating between normal pregnancies and those complicated by anencephaly. The study demonstrates the possible value of investigating other neuronal proteins which may find value as adjuncts to amniotic fluid Alpha fetoprotein levels in the prenatal diagnosis of Neural Tube Defects.

Amniotic Fluid↗

PubMed1992

Comparison of cell surface antigen HBA71 (p30/32MIC2), neuron-specific enolase, and vimentin in the immunohistochemical analysis of Ewing's sarcoma of bone.

The HBA71 antigen is an M(r) 30,000/32,000 cell surface glycoprotein (p30/32MIC2), encoded by the pseudoautosomal MIC2 gene on chromosomes X and Y, that is expressed in Ewing's sarcomas. Immunohistochemical studies demonstrate a striking specificity for HBA71 among neoplasms of diverse histologic types. In the present study, 43 cases of Ewing's sarcoma of bone were tested for HBA71 expression and six additional immunohistochemical markers regularly used in the differential diagnosis of small round-cell tumors of childhood and adolescence (neuron-specific enolase, vimentin, leukocyte common antigen, cytokeratins, muscle-specific actin, desmin). The study design included (a) random selection of Ewing's sarcoma cases from the files of Memorial Hospital beginning in 1968, (b) blind review of the original histopathologic diagnoses of ES, (c) side-by-side immunohistochemical study of recut histologic specimens, and (d) statistical analysis of immunohistochemical findings in view of clinical outcome. Of the seven antigens studied, only HBA71, neuron-specific enolase and vimentin were expressed in a significant proportion of cases. Forty-one of the 43 cases were HBA71+ (95% sensitivity); of these, 21 were neuron-specific enolase+, 29 were vimentin+, and 15 were both neuron-specific enolase+ and vimentin+. One tumor lacked all antigens, and one was vimentin+ only. Comparison of tumor tissues in five patients obtained before and after cytostatic chemotherapy showed no change in HBA71 expression or in the other antigens tested. Product-limit survival analysis (median disease-free survival was 27.3 months for the study cohort) revealed no significance of neuron-specific enolase or vimentin marker status. These results raise doubts about the usefulness of neuron-specific enolase and vimentin immunohistochemistry to distinguish Ewing's sarcoma from other small round-cell tumors of childhood and adolescence or as prognostic indicators in Ewing's sarcoma. The positive identification of Ewing's sarcoma of bone now becomes a reality using HBA71 immunohistochemistry, either as a sole method or in combination with chromosomal breakpoint analysis. This may result in achieving uniform diagnostic criteria for evaluating the biologic, therapeutic, and prognostic aspects of Ewing's sarcoma and related neoplasms.

Adolescent↗

PubMed1984

Properties and application to immunoassay of monoclonal antibodies to neuron-specific gamma gamma enolase.

Two monoclonal antibodies to human and bovine neuron-specific gamma gamma enolase have been produced in the isolated hybrid cell lines, which were obtained by fusion between gamma gamma-immunized mouse spleen cells and mouse myeloma cells (P3-NS-1/1-Ag4-1), followed by a screening procedure with an enzyme immunoassay. The monoclonal antibody to human gamma gamma enolase (E1-G3) and that to bovine gamma gamma enolase (B1-D6) consisted of gamma 2a/kappa and gamma l/kappa immunoglobulin chains, respectively. Both antibodies could bind with the respective antigen with a molar ratio of about 1:1, and were found to be specific for the gamma subunit of enolase, showing reactivities with human gamma gamma and alpha gamma, rat gamma gamma and alpha gamma, and bovine gamma gamma enolases. However, the antibodies did not cross-react with the alpha or beta subunit of human and rat enolase isozymes. Both antibodies could partially inhibit the activity of gamma gamma and alpha gamma enolases. E1-G3 antibody inhibited gamma gamma and alpha gamma enolase activity by 70 and 30%, respectively, and B1-D6 antibody, by 90 and 40%, respectively. Both antibodies had no effect on the activity of alpha alpha and beta beta enolases of human and rat origins. The applicability of E1-G3 and B1-D6 antibodies to the sandwich-type enzyme immunoassay for neuron-specific enolase (enolase gamma subunit) was examined, and it was found that the assay system using E1-G3 and B1-D6 as the labeled antibodies were sufficiently sensitive for the assay of serum neuron-specific enolase concentrations.

Animals↗

PubMed1989

Neuron-specific enolase and its mRNA are highly expressed in large congenital nevi: a study using immunocytochemistry, biochemical assay, and in situ hybridization.

The malignant transformation of congenital nevocellular nevi, both large and small, is controversial and presents problems in management. The size of the lesion is taken to indicate potential malignant transformation, but this is an arbitrary scale. A more reliable biological indicator is needed to help predict the lesions at risk. Following the localization of neuron-specific enolase to most cells of the diffuse neuroendocrine system and their neoplasms (including benign and malignant melanocytic lesions), it has been suggested that its level is related to tumor activity. In a prospective trial, the presence of neuron-specific enolase immunoreactivity, its concentration, and gene expression in nevus cells were studied in 31 congenital melanocytic nevi of various sizes (1.5 cm to bathing trunk) using immunocytochemistry, biochemical assay, and in situ hybridization. Twenty-five of the 31 congenital nevi were immunoreeactive to neuron-specific enolase antiserum, with stronger immunostaining in the larger lesions. There is an apparent linear relationship between the size of the nevi and the level of neuron-specific enolase (expressed as nanograms per milligram protein). Neuron-specific enolase mRNA was highly expressed in most of the large congenital nevi (greater than 15 cm in diameter), as revealed by autoradiography following in situ hybridization. Our results show that neuron-specific enolase and its mRNA are expressed to a greater extent in large congenital nevi compared with the smaller lesions. This might prove to be a useful indicator of those lesions at risk of malignant transformation.

Adolescent↗

PubMed1990

Immunocytochemical localization of the neuron-specific form of the c-src gene product, pp60c-src(+), in rat brain.

Neurons express high levels of a variant form of the c-src gene product, denoted pp60c-src(+), which contains a 6 amino acid insert in the amino-terminal half of the c-src protein. We have determined the localization of pp60c-src(+) in neurons using an affinity-purified anti-peptide antibody, referred to as affi-SB12, that exclusively recognizes this neuron-specific form of the c-src gene product. Using affi-SB12, we examined the distribution of pp60c-src(+) by immunoperoxidase staining of sections through adult rat brains, pp60c-src(+) was widely distributed in rat brain and appeared to be differentially expressed in subpopulations of neurons. The majority of immunoreactive neurons was found in the mesencephalon, cerebellum, pons, and medulla. Telencephalic structures that contained substantial populations of pp60c-src(+)-immunoreactive neurons included layer V of the cerebral cortex and the ventral pallidum. Within individual neurons, pp60c-src(+) immunoreactivity was localized to the cell soma and dendritic processes, while labeling of axons and nerve terminals (puncta) was not as readily detected. Dense accumulations of immunoreactive axons were rare, being most prominent in portions of the inferior and superior olive, and in the spinal trigeminal nucleus. While the regional distribution of pp60c-src(+) immunoreactivity does not correlate with any specific neuronal cell type or first messenger system, this unique pattern of expression of pp60c-src(+) suggests the existence of a previously uncharacterized functional organization within the brain. Furthermore, the localization of this neuron-specific tyrosine kinase in functionally important areas of the nerve cell, namely, dendritic processes, axons, and nerve terminals, suggests that pp60c-src(+) may regulate pleiotropic functions in specific classes of neurons in the adult central nervous system.

Animals↗

PubMed2002

[The value of specific neuronal anti-Hu antibody in the early diagnosis of small cell lung cancer].

OBJECTIVE: To evaluate the value of specific neuronal anti-Hu antibody in the early diagnosis of small cell lung cancer (SCLC). METHODS: Ninety-eight patients with SCLC were included in the study. Specific neuronal anti-Hu antibody was detected by immunohistochemistry (the ABC method) and Western blot. RESULTS: The sera from 40% (32/80) of the patients in group A (without paraneoplastic syndrome of the nervous system) reacted with the frozen sections of human cerebra and were stained by indirect immunoperoxidase method at final dilutions of 1:1,000 to 1:8,000, while the sera from 89% of the patients (16/18) in group B (with paraneoplastic syndrome of the nervous system) reacted at final dilutions of 1:1,000 to 1:64,000. Western blot analysis revealed that the specific neuronal anti-Hu antibody was identified at several bands of approximately 35,000 approximately 40,000 with nuclear extracts, and at 40,000 with HuD clonal protein. The anti-Hu antibody was detected in only two patients from group A, but in 16 patients from group B. The antibody was not detected in sera from 32 normal human subjects. CONCLUSIONS: Specific neuronal anti-Hu antibody at high titers was detected in patients with SCLC not complicated with paraneoplastic syndrome of the nervous system. This antibody may be useful in the early diagnosis of SCLC.

Adult↗

PubMed1986

An immunochemical study with neuron-specific-enolase and substance P of human enteric innervation--the normal developmental pattern and abnormal deviations in Hirschsprung's disease and pyloric stenosis.

Human enteric innervation was studied immunochemically with neuron-specific-enolase (NSE), a specific neurone marker indicative of differentiation, and substance P, a potent member of the family of neuropeptides. By examining various levels of the gut in 28 normal human fetuses of gestational ages 9 to 21 weeks, we showed that enteric neurones as a whole, as well as peptidergic neurones in particular, followed a dual gradient of development proceeding from each end to the middle of the gut. This suggests the need for caution in accepting the hypothesis of the pathogenesis of Hirschsprung's disease based on the concept of a single craniocaudal gradient of enteric neuronal development. In studies of six infants with Hirschsprung's disease, NSE immunostaining was found to be potentially useful for diagnostic purposes. NSE activity suggested that the hypertrophied nerve bundles in aganglionic bowel were metabolically active and functionally mature. Substance P-immunoreactivity was decreased in both aganglionic and distal ganglionic bowel in Hirschsprung's disease, suggesting that substance P-nerves were more extensively affected developmentally than other enteric neurones. In 28 infants with pyloric stenosis (IHPS), the presence of intense NSE activity in the ganglia in the pylorus suggested that these neurones were neither immature nor severely degenerated. A decrease in substance P immunoreactivity in IHPS suggested possible involvement of peptidergic innervation in the pathogenesis of IHPS.

Adolescent↗

PubMed1994

Comparison between normal developing striatum and developing striatal grafts using drug-induced Fos expression and neuron-specific enolase immunohistochemistry.

The cell-level functional maturation of cell suspension grafts from embryonic day 14-15 rat striatal primordia implanted unilaterally into ibotenic acid lesioned striata of adult female rats was studied from two days to 10 weeks post-grafting. The functional and morphological characteristics of the grafts were compared with those of adult grafts (one year after implantation), normal adult striata and postnatal developing striata (up to four weeks after birth). Serial sections were stained with Cresyl Violet and investigated immunohistochemically with antibodies against dopamine- and adenosine 3',5'-monophosphate-regulated phosphoprotein (DARPP-32, as a striatal marker), tyrosine hydroxylase (as a marker of dopaminergic fibres), Fos protein (as a cell-level marker of functional dopaminergic host-graft interactions), and neuron-specific enolase (correlated to differentiation and functional maturation of neuronal cells). Selected sections were double-stained for DARPP-32 and either tyrosine hydroxylase, Fos or neuron-specific enolase. The rats used to study dopamine receptor-activated expression of Fos were killed 2 h after administration of either the dopamine-releasing agent D-amphetamine (5 mg/kg intraperitoneally) or the dopamine-receptor agonist apomorphine (0.25 mg/kg subcutaneously, at which dosage it is active only on supersensitive receptors of denervated neurons). In normally developing rats, amphetamine induced Fos expression in both the striatum and globus pallidus by two weeks after birth; by four weeks, the pattern of amphetamine-induced Fos immunoreactivity was similar to that observed in adults. In the globus pallidus of both two- and three-week-old rats, amphetamine induced greater expression of Fos than in adults. Apomorphine did not induce appreciable Fos activation in either the striatum or the globus pallidus at any stage of development. In striatal grafts, amphetamine induced Fos expression from three weeks after implantation onwards, and by five to 10 weeks post-grafting the pattern of Fos immunoreactivity was similar to that observed in adult grafts. However, apomorphine induced a considerable number of Fos-positive nuclei in striatal grafts at three and four weeks after grafting. Neuron-specific enolase immunoreactivity was moderate in normal adult striatum and very high in the adult globus pallidus, and mainly located in neuronal perikarya and processes. Before two weeks of age, most neuron-specific enolase immunoreactivity was observed in internal capsule fascicles and the striatal afferents. Between two and four weeks after birth, neuron-specific enolase immunoreactivity in striatal and globus pallidus neurons gradually increased, while that in afferent fibres decreased to adult levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

PubMed1990

Activity of herpes simplex virus type 1 latency-associated transcript (LAT) promoter in neuron-derived cells: evidence for neuron specificity and for a large LAT transcript.

By using chloramphenicol acetyltransferase (CAT) assays in neuron-derived cell lines, we show here that promoter activity associated with the herpes simplex virus type 1 latency-associated transcript (LAT) had neuronal specificity. Promoter activity in these transient CAT assays coincided with a DNA region containing excellent RNA polymerase II promoter consensus sequences. Primer extension analysis in a LAT promoter-CAT plasmid construct placed the start of transcription about 28 nucleotides from the first T in the consensus TATA box sequence. Neuronal specificity of this promoter was suggested by examining the effect of sequences upstream of the promoter on CAT activity in neuronal versus nonneuronal cells. In nonneuronal cells, promoter activity was decreased 3- to 12-fold with the addition of upstream sequences. In contrast, in neuron-derived cells, the addition of upstream sequences did not decrease promoter activity. The LAT promoter predicted by our transient CAT assays was located over 660 nucleotides upstream from the 5' end of the previously mapped 2-kilobase (kb) LAT. This unusual location was explained by in situ and Northern (RNA) blot hybridization analyses that suggested that LAT transcription began near the promoter detected in our CAT assays, rather than near the 5' end of the 2-kb LAT. In situ hybridization with neurons from latently infected rabbits detected small amounts of LAT RNA within 30 nucleotides of the consensus TATA box sequence. This suggested that LAT transcription began near this TATA box. Northern blot hybridization of RNA from ganglia of latently infected rabbits revealed a faint 8.3-kb band of the same sense as LAT. We conclude that (i) the LAT promoter has neuronal specificity, (ii) the LAT promoter is located over 660 nucleotides upstream of the 5' end of the previously characterized stable 2-kb LAT, (iii) LAT transcription begins about 28 nucleotides from the first T of the consensus TATA box sequence and extends to near the first available polyadenylation site approximately 8.3 kb away, and (iv) this 8.3-kb RNA may be an unstable precursor of the more stable 2- and 1.3-kb LATs.

Animals↗

PubMed1995

c-jun inhibited the alternative splicing of neuron-specific amyloid precursor protein, but stimulated the non-neuron type one in P19 EC cells.

Three alternative splicing products of amyloid precursor protein (APP), APP770, 751 and 695, were detected in mouse embryonal carcinoma (EC) P19 cells by reverse transcriptase RNA polymerase chain reaction (RT-PCR). Alternative splicing of APP pre-mRNA in P19EC cells was remarkably changed by c-jun transformation. The relative ratio of APP770 encoding exons 7 and 8, non-neuron type, was increased by c-jun transformation, while that of APP 695 not encoding exons 7 and 8, neuron-specific one, was decreased. These results suggested that skipping of exons 7 and 8 was specifically blocked in c-jun transformed cells. APP 695, which increases in P19 EC cells under the culture conditions that induce the neuronal differentiation, did not increase in C2C5 cells under the same conditions, suggesting that c-jun transformed cells were not in the neuronal cell lineage and lost the ability to differentiate into neurons.

Alternative Splicing↗

PubMed1987

Neuron-specific enolase-positive rosettes in nephroblastoma: a possible diagnostic pitfall in aspiration cytology.

Neuron-specific enolase-positive cells, some arranged in rosettes, were identified in smears obtained in fine-needle aspiration of a left retroperitoneal tumor found in a 3-yr-old boy. Nephrectomy showed a typical nephroblastoma with a prominent blastemic component revealing a positive reaction for neuron-specific enolase in blastemic and tubular components. Neuron-specific, enolase-positive, small malignant cells are not diagnostic of neuroblastoma when coming from a tumor of the retroperitoneum even if rosettes are present.

Biopsy, Needle↗

PubMed1980

The etiology of acrylamide neuropathy: possible involvement of neuron specific enolase.

The effect of monomeric acrylamide, a potent neurotoxic agent, on total and neuron specific enolase activity was studied in vitro and in vivo. Acrylamide (10 mM) completely inhibited total enolase activity of rat brain soluble fractions. The I50 concentration was 3.7 mM. In rats chronically treated with acrylamide (550 mg/kg total) and exhibiting marked symptoms of neurotoxicity, neuron specific enolase activity was not detectable in sciatic nerves and was only 60% of control activity in brain. Total enolase activity in both central and peripheral nervous tissues was unchanged from control. The results suggest that inhibition of neuron specific enolase may be an important factor in the development of acrylamide neuropathy by interfering with glycolysis in neuronal tissue.

Acrylamides↗

PubMedDate not supplied

Heterogeneity and multiple expression of intermediate filament proteins, S-100 protein and neuron specific enolase in skin mixed tumor.

Intermediate filament proteins, keratin (KL1, PKK1, K8.12) and vimentin, S-100 protein alpha and beta subunits and neuron specific enolase were evaluated immunohistochemically to determine their distribution patterns in the tumor components of mixed tumor of skin. Keratin proteins were distributed widely in tumor epithelial cells or modified myoepithelial (MME) or neoplastic myoepithelial (NME) cells. Luminal cells of the tubulo-ductal structure of the tumor mass showed positive staining of KL1 and PKK1 keratins and an infrequently positive reaction of MoAb K8.12. The outer or basal tumor cells were characterized by coexpression of K8.12 keratin, vimentin, S-100 protein and infrequently neuron specific enolase reactivity. Heterogeneity of keratin distribution was seen in tumor epithelial cells. MME cells or NME cells of skin mixed tumor showed coexpression of keratin and vimentin, and multiple expression of intermediate filament proteins, S-100 protein and neuron specific enolase. Hyaline and chondroid changed cells stained intensely to vimentin and S-100 proteins, as well as to neuron specific enolase. The authors evaluate the histogenesis of skin mixed tumor in relation to epithelial and myoepithelial cells of the sweat gland and their immunohistochemical findings.

Adenoma, Sweat Gland↗

PubMed1995

Determination of a necdin cis-acting element required for neuron specific expression by using zebra fish.

To determine cis-acting elements required for neuron specific expression of a necdin gene, we tried to use zebra fish assay system in vivo instead of cell lines in vitro. Various expression vectors carrying upstream sequences of necdin gene fused to MEKA (lacZ) gene as a reporter were injected into fertilized zebra fish embryos and then the expression of the reporter gene was analyzed by the whole mount immunochemical method. No promoter activity was obtained with a construct carrying sequence from -63 to +63 of the necdin gene, while promoter activity with preferential skin expression was obtained with a construct having sequence from -86 to +28. Further upstream sequence from -173 to +28 exhibited neuron specific expression as well as that from -845 to +63. These results indicate that a cis-acting element responsible for neuron specific expression is located in an 87bp sequence from -173 to -87 of necdin gene.

Animals↗

PubMed1999

Neural restrictive silencer factor recruits mSin3 and histone deacetylase complex to repress neuron-specific target genes.

Accumulative evidence suggests that more than 20 neuron-specific genes are regulated by a transcriptional cis-regulatory element known as the neural restrictive silencer (NRS). A trans-acting repressor that binds the NRS, NRSF [also designated RE1-silencing transcription factor (REST)] has been cloned, but the mechanism by which it represses transcription is unknown. Here we show evidence that NRSF represses transcription of its target genes by recruiting mSin3 and histone deacetylase. Transfection experiments using a series of NRSF deletion constructs revealed the presence of two repression domains, RD-1 and RD-2, within the N- and C-terminal regions, respectively. A yeast two-hybrid screen using the RD-1 region as a bait identified a short form of mSin3B. In vitro pull-down assays and in vivo immunoprecipitation-Western analyses revealed a specific interaction between NRSF-RD1 and mSin3 PAH1-PAH2 domains. Furthermore, NRSF and mSin3 formed a complex with histone deacetylase 1, suggesting that NRSF-mediated repression involves histone deacetylation. When the deacetylation of histones was inhibited by tricostatin A in non-neuronal cells, mRNAs encoding several neuronal-specific genes such as SCG10, NMDAR1, and choline acetyltransferase became detectable. These results indicate that NRSF recruits mSin3 and histone deacetylase 1 to silence neural-specific genes and suggest further that repression of histone deacetylation is crucial for transcriptional activation of neural-specific genes during neuronal terminal differentiation.

3T3 Cells↗

PubMed1991

[Effect of triiodothyronine on the expression of neuron-specific enolase activity in developing cultured human fetal cerebral neurons].

Culture of human fetal cerebral neurons in serum-free medium was established. The enolase isoenzymes in the cultured neurons were fractionated by DEAE cellulose ion exchange chromatography. The total enolase activity was resolved into three peaks: Non-neuronal enolase (NNE or alpha alpha and alpha gamma) appeared in 10-day cultures, and the peak of neuron -specific enolase (NSE or gamma gamma) in the group added T3 appeared earlier (in 15-day cultures) than in the control group (20-day cultures). The percentage of gamma gamma enolase activity in the group added T3 was 2.55 times higher than that in the control group. In conclusion, the present study demonstrated that T3 in physiological concentration may promote the differentiation and maturation of neurons in cultures, verifying the expression of NSE and the switch-over of NNE (alpha alpha, alpha gamma) to NSE (gamma gamma).

Brain↗