Roles of NG2 Glia in Cerebral Small Vessel Disease / 神经科学通报·英文版

Cerebral small vessel disease (CSVD) is one of the most prevalent pathologic processes affecting 5% of people over 50 years of age and contributing to 45% of dementia cases. Increasing evidence has demonstrated the pathological roles of chronic hypoperfusion, impaired cerebral vascular reactivity, and leakage of the blood-brain barrier in CSVD. However, the pathogenesis of CSVD remains elusive thus far, and no radical treatment has been developed. NG2 glia, also known as oligodendrocyte precursor cells, are the fourth type of glial cell in addition to astrocytes, microglia, and oligodendrocytes in the mammalian central nervous system. Many novel functions for NG2 glia in physiological and pathological states have recently been revealed. In this review, we discuss the role of NG2 glia in CSVD and the underlying mechanisms.

The Oncogenesis of Glial Cells in Diffuse Gliomas and Clinical Opportunities / 神经科学通报·英文版

Glioma is the most common and lethal intrinsic primary tumor of the brain. Its controversial origins may contribute to its heterogeneity, creating challenges and difficulties in the development of therapies. Among the components constituting tumors, glioma stem cells are highly plastic subpopulations that are thought to be the site of tumor initiation. Neural stem cells/progenitor cells and oligodendrocyte progenitor cells are possible lineage groups populating the bulk of the tumor, in which gene mutations related to cell-cycle or metabolic enzymes dramatically affect this transformation. Novel approaches have revealed the tumor-promoting properties of distinct tumor cell states, glial, neural, and immune cell populations in the tumor microenvironment. Communication between tumor cells and other normal cells manipulate tumor progression and influence sensitivity to therapy. Here, we discuss the heterogeneity and relevant functions of tumor cell state, microglia, monocyte-derived macrophages, and neurons in glioma, highlighting their bilateral effects on tumors. Finally, we describe potential therapeutic approaches and targets beyond standard treatments.

Immunological Markers for Central Nervous System Glia / 神经科学通报·英文版

Glial cells in the central nervous system (CNS) are composed of oligodendrocytes, astrocytes and microglia. They contribute more than half of the total cells of the CNS, and are essential for neural development and functioning. Studies on the fate specification, differentiation, and functional diversification of glial cells mainly rely on the proper use of cell- or stage-specific molecular markers. However, as cellular markers often exhibit different specificity and sensitivity, careful consideration must be given prior to their application to avoid possible confusion. Here, we provide an updated overview of a list of well-established immunological markers for the labeling of central glia, and discuss the cell-type specificity and stage dependency of their expression.

Electroacupuncture Alleviates Functional Constipation in Mice by Activating Enteric Glial Cell Autophagy via PI3K/AKT/mTOR Signaling / 中国结合医学杂志

OBJECTIVE@#To investigate autophagy-related mechanisms of electroacupuncture (EA) action in improving gastrointestinal motility in mice with functional constipation (FC).@*METHODS@#According to a random number table, the Kunming mice were divided into the normal control, FC and EA groups in Experiment I. The autophagy inhibitor 3-methyladenine (3-MA) was used to observe whether it antagonized the effects of EA in Experiment II. An FC model was established by diphenoxylate gavage. Then the mice were treated with EA stimulation at Tianshu (ST 25) and Shangjuxu (ST 37) acupoints. The first black stool defecation time, the number, weight, and water content of 8-h feces, and intestinal transit rate were used to assess intestinal transit. Colonic tissues underwent histopathological assessment, and the expressions of autophagy markers microtubule-associated protein 1 light chain 3 (LC3) and Beclin-1 were detected by immunohistochemical staining. The expressions of phosphoinositide 3-kinases (PI3K)-protein kinase B (AKT)-mammalian target of rapamycin (mTOR) signaling pathway members were investigated by Western blot and quantitative reverse transcription-polymerase chain reaction, respectively. The relationship between enteric glial cells (EGCs) and autophagy was observed by confocal immunofluorescence microscopy, localization analysis, and electron microscopy.@*RESULTS@#EA treatment shortened the first black stool defecation time, increased the number, weight, and water content of 8-h feces, and improved the intestinal transit rate in FC mice (P<0.01). In terms of a putative autophagy mechanism, EA treatment promoted the expressions of LC3 and Beclin-1 proteins in the colonic tissue of FC mice (P<0.05), with glial fibrillary acidic protein (GFAP) and LC3 significantly colocalized. Furthermore, EA promoted colonic autophagy in FC mice by inhibiting PI3K/AKT/mTOR signaling (P<0.05 or P<0.01). The positive effect of EA on intestinal motility in FC mice was blocked by 3-MA.@*CONCLUSION@#EA treatment can inhibit PI3K/AKT/mTOR signaling in the colonic tissues of FC mice, thereby promoting EGCs autophagy to improve intestinal motility.

Effects of benzo(a)pyrene on expressions of insulin-degrading enzyme and neprilysin in neuroglia cells / 北京大学学报(医学版)

OBJECTIVE@#To investigate effects of benzo(a)pyrene (BaP) on expressions of insulin-degrading enzyme (IDE) and neprilysin (NEP) which have the ability to degrade β-amyloid (Aβ) in neuroglia cells.@*METHODS@#Primary mix-neuroglia cells were cultured from newborn SD rats. After exposure to BaP, Aβ1-42 oligomer or Aβ1-42 fiber individually or jointly for 24 h, the cell survival rate was measured by cell counting kit-8 (CCK-8). Afterwards, the primary mix-neuroglia cells were divided randomly into six groups: Control group, BaP group (2.00 μmol/L), Aβ1-42 oligomer group (20.00 mg/L), BaP plus Aβ1-42 oligomer group, Aβ1-42 fiber group (20.00 mg/L) and BaP plus Aβ1-42 fiber group, of which BaP was pretreated for 12 h followed by cotreatment with different aggregated Aβ1-42. The expressions of IDE and NEP were measured by quantitative real-time polymerase chain reaction (qRT-PCR) for mRNA level and Western blotting for protein level.@*RESULTS@#The cell survival rate showed no significant differences after treatment with BaP (≤20.00 μmol/L), Aβ1-42 oligomer (20.00, 40.00 mg/L), Aβ1-42 fiber (20.00, 40.00 mg/L) or cotreatment with BaP and Aβ1-42 oligomer or BaP and Aβ1-42 fiber. Compared with the control group, expressions of IDE and NEP in BaP-treated alone group had no obvious change; however, exposure to Aβ1-42 oligomer alone significantly increased the mRNA and protein level of IDE (P<0.05), and the BaP pretreatment could significantly inhibit the up-regulated expressions of IDE by Aβ1-42 oligomer (P<0.05); on the other hand, exposure either to Aβ1-42 fiber alone or under the BaP pretreatment did not change the mRNA and protein level of IDE and NEP obviously.@*CONCLUSION@#On the premise of no significant change of cell survival rate, BaP pretreatment inhibited the up-regulated expressions of IDE in primary mixed neuroglia cells under cotreatment with Aβ oligomer, indicating that BaP may disturb degradation of Aβ oligomer and cause deposition of β-amyloid and further induce cognitive decline and acceleration of Alzheimer.

Immunohistochemical analysis of retinoblastoma cell phenotype using neuronal and glial cell markers / Análise imuno-histoquímica do fenótipo de células de retinoblastoma utilizando marcadores de células neuronais e gliais

ABSTRACT Purpose: The cellular origin of retinoblastoma is uncertain as constituent tumor cells heterogeneously express markers of both immature and mature retinal cells. An immunohistochemical analysis of cellular origin may yield valuable insights into disease progression and treatment options. This study aimed to determine the cellular origin of retinoblastoma in a large case series and correlate these findings with histopathological prognostic factors. Methods: Thirty-nine retinoblastoma cases were histopathologically diagnosed and analyzed by immunohistochemistry using monoclonal antibodies against the immature neural cell marker SRY-box containing gene 2 (SOX-2), the mature neuronal cell marker microtubule-associated protein 2 (MAP2), and the mature glial cell marker glial fibrillary acidic protein (GFAP). Histopathological features were also evaluated, including patterns of growth, differentiation, vitreous seeding, and choroidal/scleral, optic nerve, and anterior chamber invasion. Two retinoblastoma cell lines, WERI-1 and Y79, were studied by immunocytochemistry using the same antibodies. Results: Expression of SOX-2 was strong in 97.4% of retinoblastoma cases, while MAP-2 was expressed in 59% of cases. Immunostaining for GFAP was positive only in reactive stromal astrocytes interspersed amongst tumor cells and in peritumoral tissue. There was no correlation between histopathological prognostic factors and immunohistochemical markers. Retinoblastoma cell lines showed strong positivity for SOX2 (90% of WERI-1 cells and 70% of Y79 cells) and MAP2 (90% of cells in both lines). GFAP was completely negative in both cell lines. Conclusion: The majority of retinoblastomas and both RB cell lines expressed an immature neural and/or a mature neuronal cell marker, but not a glial marker. These results indicate a typical neuroblast or neuronal origin and eliminate astrocyte differentiation from neural stem cells as the source of retinoblastoma.

RESUMO Objetivos: Este estudo visa determinar a origem do retinoblastoma em um número de casos e correlacionar essos achados com fatores prognósticos e histopatológicos conhecidos. Métodos: Trinta e nove casos de retinoblastoma foram diagnosticados e analisados com imuno-histoquímica usando marcadores de anticorpos monoclonais contra as células de retina imaturas (SOX-2: SRY-box containing gene 2), contra as células da retina maturas (MAP2: microtubule -associated protein 2) e contra as células gliais maturas (GFAP: glial fibrillar acidic protein). Foram avaliadas características microscópicas dos casos (grau de diferenciação, presença de semeadura vítrea, invasão de coroide/esclera, nervo óptico e câmara anterior). Duas linhas celulares de retinoblastoma (WERI-1 e Y79) também foram testadas, utilizando os três marcadores. Resultados: A expressão de SOX-2 foi positiva em 97,4% dos casos de retinoblastoma, enquanto MAP2 foi positivo em 59% dos casos. GFAP foi apenas positivo no estroma (astrócitos reativos). Não houve correlação entre preditores histopatológicos e marcadores imunohistoquímicos avaliados. As linhagens celulares mostraram positividade para SOX-2 (90% em WERI-1 e 70% das células Y79). Ambas as linhagens celulares se mostraram fortemente positivas con MAP2 (90%), enquanto não houve expressão de GFAP em nenhuma das linhas celulares estudadas. Conclusões: A maioria das células de retinoblastoma desta série de casos expressa marcadores de células retinianas imaturas, além de marcadores de células maduras. As linhas celulares Y79 e WERI-1 apresentaram imunomarcação para ambos os marcadores neurais em percentagens semelhantes a dos casos avaliados. Portanto, estes resultados confirmam a origem neural do tumor em particular. Alem disso, a ausência de células positivas para GFAP no tumor descarta diferenciação de astrócitos em retinoblastoma.

Osteonecrosis Related to Once-Yearly Zoledronic Acid Treatment in an Osteoporotic Patient after Dental Implant

This paper presents a case of osteonecrosis of the jaw related to zoledronic acid (5 mg) administered once yearly to treat osteoporosis. A 79-year-old woman who has been treated for osteoporosis for 5 years with 5 applications of zoledronic acid was referred for evaluation. The patient had been submitted to dental implant placement and there was no osseointegration. On clinical examination, suppuration and exposed bone on the alveolar ridge were observed. Radiographic examination revealed an osteolytic area and bone sequestration. Both clinical and radiological features were suggestive of osteonecrosis. The treatment consisted of surgery to remove the affected bone completely. The patient is asymptomatic at 9 months after surgery. Dentists and oral surgeons should be alert to the possibility of osteonecrosis related to the use of once-yearly injections of zoledronic acid for the treatment of postmenopausal osteoporosis.

O presente estudo teve como objetivo apresentar um caso de osteonecrose dos maxilares associada ao uso de ácido zoledrônico (5 mg) administrado uma vez ao ano para tratar a osteoporose. Uma mulher de 79 anos de idade estava em tratamento de osteoporose por 5 anos com 5 aplicações do ácido zoledrônico foi encaminhada para nossa avaliação. A paciente tinha sido submetida à colocação de implante dental e não houve osseointegração. Ao exame clínico, supuração e osso exposto no rebordo alveolar foram observados. Os exames radiográficos revelaram uma área osteolítica e sequestro ósseo. Ambos os aspectos clínicos e radiográficos eram sugestivos de osteonecrose. O tratamento consistiu de cirurgia para remover todo o osso afetado. A paciente está assintomática há 9 meses (desde a cirurgia). Cirurgiões-dentistas e cirurgiões orais devem estar atentos para a possibilidade de osteonecrose relacionada ao uso de injeções anuais de ácido zoledrônico para tratamento da osteoporose pós-menopausa.

Proteomics analysis of human brain glial cell proteome by 2D gel.

INTRODUCTION: Proteomics is increasingly employed in both neurological and oncological research, and applied widely in every area of neuroscience research including brain cancer. Astrocytomas are the most common glioma and can occur in most parts of the brain and occasionally in the spinal cord. Patients with high‑grade astrocytomas have a life expectancy of <1 year even after surgery, chemotherapy, and radiotherapy. MATERIALS AND METHODS: We extracted proteins from tumors and normal brain tissues and then evaluated the protein purity by Bradford test and spectrophotometry method. In this study, we separated proteins by the two‑dimensional (2DG) gel electrophoresis method, and the spots were analyzed and compared using statistical data. RESULTS: On each analytical 2D gel, an average of 800 spots was observed. In this study, 164 spots exhibited up‑regulation of expression level, whereas the remaining 179 spots decreased in astrocytoma tumor relative to normal tissue. Results demonstrate that functional clustering and principal component analysis (PCA) has considerable merits in aiding the interpretation of proteomic data. Proteomics is a powerful tool in identifying multiple proteins that are altered following a neuropharmacological intervention in a disease of the central nervous system (CNS). CONCLUSION: 2‑D gel and cluster analysis have important roles in the diagnostic management of astrocytoma patients, providing insight into tumor biology. The application of proteomics to CNS research has invariably been very successful in yielding large amounts of data.

Immunohistochemical evaluation of the goat forestomach during prenatal development

Here we report the detection and distribution of synaptophysin (SPY), non-neuronal enolase (NNE), glial fibrillary acidic protein (GFAP), vimentin (VIM), neuropeptide Y (NPY), and vasoactive intestinal peptide (VIP) expression in the goat forestomach during prenatal development. A total of 140 embryos and fetuses were examined to evaluate protein expression from the first stage of prenatal life until birth. In all cases, SPY immunoreactivity was detected at 53 days gestation in the lamina propria-submucosa, tunica muscularis, serosa, and myenteric plexuses. Immunoreactivity to NNE was observed at 64 days gestation in the same locations as well as the epithelial layer. Glial cells were found at 64 days as indicated by signals corresponding to GFAP and VIM at 39 days. Positive staining for NPY and VIP was observed at 113, 75, and 95 days in the rumen, reticulum, and omasum, respectively, in the lamina propria-submucosa, tunica muscularis, and myenteric plexuses of each of these gastric compartments. These findings indicate possible preparation of the fetal goat forestomach for postnatal function. Compared to other ruminant species, neuroendocrine cells, glial cells and peptidergic innervations markers were detected earlier compared to sheep but at around the same stage as in deer.

Glial cell activity is maintained during prolonged inflammatory challenge in rats

We evaluated the expression of glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), ionized calcium binding adaptor protein-1 (Iba-1), and ferritin in rats after single or repeated lipopolysaccharide (LPS) treatment, which is known to induce endotoxin tolerance and glial activation. Male Wistar rats (200-250 g) received ip injections of LPS (100 µg/kg) or saline for 6 days: 6 saline (N = 5), 5 saline + 1 LPS (N = 6) and 6 LPS (N = 6). After the sixth injection, the rats were perfused and the brains were collected for immunohistochemistry. After a single LPS dose, the number of GFAP-positive cells increased in the hypothalamic arcuate nucleus (ARC; 1 LPS: 35.6 ± 1.4 vs control: 23.1 ± 2.5) and hippocampus (1 LPS: 165.0 ± 3.0 vs control: 137.5 ± 2.5), and interestingly, 6 LPS injections further increased GFAP expression in these regions (ARC = 52.5 ± 4.3; hippocampus = 182.2 ± 4.1). We found a higher GS expression only in the hippocampus of the 6 LPS injections group (56.6 ± 0.8 vs 46.7 ± 1.9). Ferritin-positive cells increased similarly in the hippocampus of rats treated with a single (49.2 ± 1.7 vs 28.1 ± 1.9) or repeated (47.6 ± 1.1 vs 28.1 ± 1.9) LPS dose. Single LPS enhanced Iba-1 in the paraventricular nucleus (PVN: 92.8 ± 4.1 vs 65.2 ± 2.2) and hippocampus (99.4 ± 4.4 vs 73.8 ± 2.1), but had no effect in the retrochiasmatic nucleus (RCA) and ARC. Interestingly, 6 LPS increased the Iba-1 expression in these hypothalamic and hippocampal regions (RCA: 57.8 ± 4.6 vs 36.6 ± 2.2; ARC: 62.4 ± 6.0 vs 37.0 ± 2.2; PVN: 100.7 ± 4.4 vs 65.2 ± 2.2; hippocampus: 123.0 ± 3.8 vs 73.8 ± 2.1). The results suggest that repeated LPS treatment stimulates the expression of glial activation markers, protecting neuronal activity during prolonged inflammatory challenges.

Nestin down-regulation of cortical radial glia is delayed in rats submitted to recurrent status epilepticus during early postnatal life / Atraso no desaparecimento da nestina na glia radial cortical de ratos submetidos a recorrentes status epilepticus durante o desenvolvimento pós-natal precoce

OBJECTIVE: Nestin is temporarily expressed in several tissues during development and it is replaced by other protein types during cell differentiation process. This unique property allows distinguishing between undifferentiated and differentiated cells. This study was delineated to analyze the temporal pattern of nestin expression in cortical radial glial cells of rats during normal development and of rats submitted to recurrent status epilepticus (SE) in early postnatal life (P). METHOD: Experimental rats were submitted to pilocarpine-induced SE on P7-9. The cortical temporal profile of nestin was studied by immunohistochemistry at multiple time points (P9, P10, P12, P16, P30 and P90). RESULTS: We observed delayed nestin down-regulation in experimental rats of P9, P10, P12 and P16 groups. In addition, few radial glial cells were still present only in P21 experimental rats. CONCLUSION: Our results suggested that SE during early postnatal life alters normal maturation during a critical period of brain development.

OBJETIVO: A nestina, temporariamente expressa em diversos tecidos durante o desenvolvimento, é substituída no processo de diferenciação celular, o que permite a distinção entre células diferenciadas e indiferenciadas. O objetivo deste estudo foi verificar o padrão temporal da expressão da nestina nas células da glia radial cortical de ratos durante o desenvolvimento normal e nos ratos submetidos a sucessivos status epilepticus (SE) no periodo pós-natal precoce (P). MÉTODO: Os animais foram submetidos ao SE induzido pela pilocarpina em P7-9. O perfil temporal da nestina foi estudado por imuno-histoquímica em P9, P10, P12, P16, P30 e P90. RESULTADOS: Nos ratos experimentais, observamos atraso no desaparecimento da nestina nos grupos P9, P10, P12 e P16. Ainda, encontramos algumas glias radiais corticais apenas em P21 experimental. CONCLUSÃO: Nossos resultados sugerem que o SE durante o desenvolvimento pós-natal precoce altera o processo de maturação durante um periodo crítico do desenvolvimento encefálico.

Efeitos da nicotina e/ou etanol no hipocampo de camundongos adolescentes: morte celular e densidade neuronal e glial ao final da exposição e após a retirada das drogas / Effects of nicotine and/or ethanol in the hippocampus of adolescent mice: cell death and neuronal and glial densities at the end of exposure and during drugs withdrawal

Fumar e consumir bebidas alcoólicas estão frequentemente associados durante a adolescência. Contudo, poucos estudos em modelos animais têm como foco as bases neurobiológicas da exposição combinada à nicotina e ao etanol no cérebro de adolescentes. Nesse estudo investigamos morte celular e alterações na densidade neuronal e glial nas regiões granulosa do giro denteado (GrDG), camada molecular (Mol), CA1, CA2 e CA3 do hipocampo, durante a exposição e dois e cinco dias após o seu término. Para tanto, do 30º ao 45º dia pós-natal (PN30-PN45), 233 camundongos C57BL/6 machos e fêmeas foram expostos à nicotina (NIC) e /ou etanol (ETOH). Assim, quatro grupos experimentais foram utilizados: 1) NIC+ETOH: exposição concomitante a NIC (50ug/ml em 2% de sacarina na água de beber) e ETOH (25%, 2g/kg i.p. em dias alternados), 2) exposição à NIC, 3) exposição ao ETOH, 4) exposição ao veículo. Avaliamos morte celular por apoptose pela técnica do TUNEL, densidades neuronal e glial pelo método do Disector óptico e espessuras das regiões durante a exposição (PN45) e dois (PN47) e cinco dias (PN50) após o seu término. ANOVAS foram utilizadas para detectar efeitos do tratamento e/ou interações do tratamento com outros fatores. O grau de significância assumido foi de p<0.05. Em PN45, a exposição ao etanol aumentou o número de células TUNEL+ em todas as regiões hipocampais quando comparado ao grupo veículo e a nicotina provocou uma resposta menos severa e dependente da região. Os animais que receberam nicotina+etanol não diferiram dos animais veículo em todas as regiões hipocampais. Em PN47, ainda foi identificado aumento no número de células TUNEL+ nos grupos ETOH e NIC, mas em menor magnitude que os efeitos identificados durante a exposição. Esses resultados foram acompanhados por redução das densidades neuronal e glial em todos os grupos tratados. Em PN50, a abstinência de nicotina e/ou etanol foi associada com reduções compensatórias de células TUNEL+...

Smoking and consumption of alcoholic beverages are frequently associated during adolescence. However, there have been few animal studies on the neurobiological bases of the combined exposure in the adolescent brain. In the present study, we investigated the effects of adolescent nicotine and/or ethanol exposure and withdrawal on the following regions of the hippocampus: Granular layer of the Dentate Gyrus (GrDG), Molecular layer (Mol), CA1, CA2 and CA3. From the 30th to the 45th postnatal day (PN30-PN45), 233 C57BL/6 male and female mice were exposed to nicotine free base (NIC) and/or ethanol (ETOH). Four groups were analyzed: 1) concomitant NIC (50 ug/ml in 2% saccharin to drink) and ETOH (25%, 2 g/kg i.p. injected every other day) exposure; 2) NIC exposure; 3) ETOH exposure; 4) vehicle. We evaluated cell degeneration (TUNEL assay), neuronal and glial densities (optical Disector) and region thicknesses during the exposure (PN45) and two (PN47) and five (PN50) days post-exposure. ANOVAs were used to identify treatment effects and/or interactions with other factors. Significance was assumed at the level of p<0.05. On PN45, ETOH elicited an increase in the number of TUNEL+ cells relative to the vehicle group in all hippocampal regions. NIC elicited less severe region-dependent effects. Concomitant NIC and ETOH failed to elicit significant changes in the number of TUNEL+ cells. On PN47, the effects were similar to those described for PNB45, even though smaller in magnitude. These results were paralleled by reductions in neuronal and glial cells densities for all treatment groups. In contrast, on PN50, ethanol and/or nicotine withdrawal were associated with compensatory reductions in TUNEL+ cells in all hippocampal regions. These results were paralleled by a reversal of effects on neuronal and glial densities. There were no effects on region thicknesses both during exposure and withdrawal. These results suggest that deleterious effects of nicotine...

Time-dependent expression of astroglial S100beta following diffuse brain injury in rats / 法医学杂志

OBJECTIVE@#To investigate the dynamics of the induction of S100beta in different parts of rat brain following the diffuse brain injury.@*METHODS@#Immunohistochemistry and auto-image analysis were to determine the expression of astroglial S100beta after diffuse brain injury in rats. Forty rats were distributed into groups according to injury time of 30min, and2,4,12,24h, and 3,6 d after diffuse brain injury, and normal rats as control.@*RESULTS@#The number of S100beta positive cells in the four areas increased significantly followed by a decrease, and then a further increase. The expression of S100beta could be detected increasing in 2h, and increased significantly in 4h, and it reached apex 12h after DBI, and decreased gradually to the level less than normal 3d, and returned to normal 7d following injury. In the postmortem injury groups, there were no significant changes in anti-S100beta immunoreactivities in four areas of brain compared to the control group.@*CONCLUSION@#The present study showed the time-dependent expression of S100beta is obvious following diffuse brain injury, and suggested S100beta be suitable as a marker for brain injury age determination.

Changes of cyclin D1 expression following human brain contusion / 法医学杂志

OBJECTIVE@#To study the relationships of Cyclin D1 expression with the posttraumatic intervals (PTI) following the cerebra, brainstem or cerebella contusion in human.@*METHODS@#88 cases of brain contusions of the closed head injury were investigated with pathological and Cyclin D1 immunohistochemistry methods. The results were analyzed by image analysis technique (IAT).@*RESULTS@#The immunoreactivity of Cyclin D1 was almost disappeared in the core cells of the brain contusion. Cyclin D1-positive cells started to increase in the boundary of the brain contusion in the 1h group. Cyclin D1-positive cells were increased significantly in the 3 h-30 d groups and maintained at a high level in the boundary of the brain contusion of those groups. It is suggested that the Cyclin D1-positive cells were primarily origin from microglia and other glia. A few neurons expressed Cyclin D1.@*CONCLUSION@#Cyclin D1 can express in several kinds of brain cells following the contusion, especially in the glia cells. Cyclin D1-positive cells were increased obviously and rapidly after injury, so it could be used as a reference marker for early stage brain injury.

The research progression of S100beta as a neurochemistry maker / 法医学杂志

S100beta is one kind of the calcium binding proteins. As growth factor of neuraxon, it is excreted by neuroglial cell, and distributing in nerve tissue extensively. Although S100beta has very important values neurophysiological, it also has neurotoxicity with excreting overmuch. Concentration of S100beta changes regularity in serum after the brain injury. In addition, it has a close relations with the degree of brain damage, which can be regarded as the neural new marker of biochemistry after brain damage. The advances of S100beta protein, in the research on neurophysiological values and its application for nerve tissue injury, disease were reviewed.

Increased expression of osteopontin in the spinal cords of Lewis rats with experimental autoimmune neuritis

To investigate the pattern of expression of osteopontin (OPN) in tissues of the central nervous system (CNS) responding to peripheral immunological stimulation, the expression of OPN was studied in the spinal cord of rats with experimental autoimmune neuritis (EAN). In this model system, the sciatic nerves and spinal nerve roots are the target organs of EAN and the spinal cord is a remote organ that may be indirectly affected. OPN was constitutively expressed in some astrocytes adjacent to the pia mater and neurons in normal rats. In rats with EAN, OPN was increased in the same cells and in some inflammatory cells, including macrophages in the subarachnoid space. Expression of CD44, a receptor of OPN, was weak in normal spinal cord tissue and increased in the entire spinal cord parenchyma in rats with EAN, as well as in inflammatory cells. These findings suggest that inflammatory cells as well as reactive astrocytes are major sources of OPN and CD44 in the spinal cord of rats with EAN. Further study is needed to elucidate the functional role of OPN in the spinal cord affected by EAN.

A study of the relation between interval of the injury and the reaction of neurons, glial cells after experimental brain contusion / 法医学杂志

OBJECTIVE@#To observe the change of c-fos protein(Fos) and nerve growth factor receptor (NGFR) staining in the brain of rat after experimental brain contusion.@*METHODS@#Immunohistochemistry of c-fos and NGFR were applied to investigate the brain contusion.@*RESULTS@#(1) The expression of Fos protein could be observed at 0.5 h after injury and then increased with the prolonging of time. By 3 h after injury, the positive staining cells could be detected massively not only in and round the wound site but also in other areas of the whole ipsilateral cortex. The stains decreased 6-12 h later and could hardly be detected 1 d after the brain contusion. The control-experiment is negative. (2) NGFR positive staining cells could be found round the wound area 1 d postlesion. At 3 d following injury, a peak of massive positively stained cells appeared both in number and in intensity, showing significant differences compare with that of 1 d after damage (P < 0.01). 5 d later the positive express declined slowly. The express in the control-rat is negative.@*CONCLUSION@#There is a rule that the expression of Fos and NGFR positive staining changes with time going after brain contusion, which will be of great value in estimation of brain injury time. Detection of Fos can be used for time deduction in earlier period after injury, while NGFR in later period. They are also very important for distinguishing between antemortem or postmortem injury.

Macroglia cells of the macaque monkey retina

There are two types of macroglia cells in the macaque monkey retina: Müller cells and astrocytes. Both cell types are in close contact with neuronal structures as well as with the retinal vasculature and are thus well suited for their many physiological tasks. Müller cells ubiquitously traverse the whole thickness of the retina whereas astrocytes are only found in the ganglion cell and nerve fiber layers of vascularized retinal regions. In the adult, astrocytes are very scarce in the central 4mm around the fovea, a region coinciding with peak Müller cell densities. During development this area is transiently occupied by astrocytes which then disappear during the first postnatal weeks at least in part through apoptosis. Possible reasons for this transiency will be discussed.

The extracellular matrix of the midline and non-midline midbrain glia: correlations with neurite growth-supporting abilities

The central nervous system (CNS) midline plays an important role in growth and guidance of axons. At the midline, a multiplicity of cell types establish boundaries that control the navigation of crossed and uncrossed axonal fibers. The extracellular matrix (ECM) molecules of the resident neuroepithelial or committed neuronal of glial cells could be involved in the control of axon growth and axon guidance. This review reports the recent advances in the study of the structure and functional role of the ECM at the midline locus of the CNS. In vivo and in vitro approaches are considered to provide new clues in the understanding of processes involved in the cellular decisions of the CNS midline.