• MeSH
• neurodegenerativní nemoci patologie   MeSH
• oligodendroglie fyziologie   patologie   MeSH
• Publikační typ
• rozhovory MeSH

NG2 cells represent one of the most proliferative glial cell populations in the intact mammalian central nervous system (CNS). They are well-known for their ability to renew themselves or to generate new oligodendrocytes during development as well as in adulthood, therefore also being termed oligodendrocyte progenitor cells. Following CNS injuries, such as demyelination, trauma or ischemia, the proliferative capacity of NG2 cells rapidly increases and moreover, their differentiation potential broadens, as documented by numerous reports also describing their differentiation into astrocytes or even neurons. Here, we summarize the current knowledge about NG2 cells proliferation, their fate plasticity during embryogenesis as well as in postnatal CNS under physiological and pathological conditions, with the main emphasis on the role of various signaling molecules, growth factors, hormones or even neurotransmitters on the fate potential of NG2 cells.

• MeSH
• antigeny metabolismus   MeSH
• kmenové buňky účinky léků   fyziologie   MeSH
• látky ovlivňující centrální nervový systém farmakologie   terapeutické užití   MeSH
• lidé MeSH
• mezibuněčné signální peptidy a proteiny metabolismus   MeSH
• multipotentní kmenové buňky účinky léků   fyziologie   transplantace   MeSH
• neurogeneze účinky léků   fyziologie   MeSH
• neuroglie účinky léků   fyziologie   MeSH
• neuroplasticita účinky léků   fyziologie   MeSH
• oligodendroglie účinky léků   fyziologie   MeSH
• proliferace buněk účinky léků   fyziologie   MeSH
• proteoglykany metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Alzheimerova choroba je závažné neurodegenerativní one­mocnění a nejčastější příčina demence v populaci nad 60 let. Ukládání betaamyloidu a tvorba neurofibrilárních klubek v mozku předchází vznik demence o mnoho let. Neúspěch léčby omezující ukládání betaamyloidu vede k přehodnocování teorií o patofyziologii tohoto onemocnění. V této souvislosti se výzkum zaměřuje na roli zánětu jako spouštěcího momentu i doprovodného procesu neurodegenerace. V našem článku shrneme některé poznatky týkající se imunitních funkcí jednotlivých buněk mozku a jejich vztahu ke vzniku a rozvoji Alzheimerovy choroby ve světle hypotézy imunitní reakce.

Alzheimer's disease is a severe neurodegenerative disorder and the most common cause of dementia in the population above 60 years of age. Beta-amyloid accumulation and neurofibrillary tangles formation in the brain precedes the development of Alzheimer's dementia by many years. As beta-amyloid accumulation inhibition failed as a treatment option, the theories on the Alzheimer's disease pathophysio­lo­gy are being revised. In this context, research targets the role of inflammation as the possible trigger mechanism and accompanying process of neurodegeneration. This article summarizes some knowledge of the immune function of brain cells and its potential relation to Alzheimer's disease progression in the light of the immune reaction hypothesis.

• Klíčová slova
• imunitní odpověď,
• MeSH
• aktivace komplementu imunologie   MeSH
• Alzheimerova nemoc * etiologie   imunologie   patofyziologie   MeSH
• astrocyty fyziologie   imunologie   MeSH
• centrální nervový systém imunologie   MeSH
• imunitní systém - jevy * MeSH
• lidé MeSH
• membranolytický komplex MeSH
• mikroglie fyziologie   imunologie   MeSH
• neurony MeSH
• oligodendroglie fyziologie   MeSH
• zánět * imunologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

Over a century ago, hyperplasia and hypertrophy of astrocytes was noted as a histopathological hallmark of multiple sclerosis and was hypothesized to play an important role in the development and course of this disease. However until today, the factual contribution of astrocytes to multiple sclerosis is elusive. Astrocytes may play an active role during degeneration and demyelination by controlling local inflammation in the CNS, provoking damage of oligodendrocytes and axons, and glial scarring but might also be beneficial by creating a permissive environment for remyelination and oligodendrocyte precursor migration, proliferation, and differentiation. Recent findings from our lab suggest that brain lipid binding protein (FABP7) is implicated in the course of multiple sclerosis and the regulation of astrocyte function. The relevance of our findings and data from other groups are highlighted and discussed in this paper in the context of myelin repair.

• MeSH
• astrocyty cytologie   fyziologie   chemie   MeSH
• axony fyziologie   patologie   MeSH
• centrální nervový systém patofyziologie   patologie   MeSH
• demyelinizační nemoci diagnóza   etiologie   patologie   MeSH
• fyziologie buňky fyziologie   MeSH
• lidé MeSH
• metaanalýza jako téma MeSH
• myelinové proteiny chemie   metabolismus   MeSH
• myši MeSH
• nádorové supresorové proteiny fyziologie   chemie   MeSH
• oligodendroglie cytologie   fyziologie   patologie   MeSH
• poranění mozku patofyziologie   patologie   MeSH
• regenerace fyziologie   imunologie   MeSH
• roztroušená skleróza etiologie   patofyziologie   patologie   MeSH
• transportní proteiny fyziologie   chemie   MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• Publikační typ
• přehledy MeSH

• MeSH
• astrocyty fyziologie   imunologie   patologie   MeSH
• biologické markery MeSH
• chondroitinasa ABC MeSH
• chondroitinlyasy genetika   izolace a purifikace   metabolismus   MeSH
• experimenty na zvířatech MeSH
• financování organizované MeSH
• imunochemie metody   normy   MeSH
• neurony fyziologie   imunologie   patologie   MeSH
• oligodendroglie fyziologie   imunologie   patologie   MeSH
• poranění míchy enzymologie   genetika   MeSH
• potkani Wistar MeSH
• statistika jako téma MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH

The neurosphere assay has been used to maintain neural progenitor cells (NPCs) in the undifferentiated state. These cells are multipotent and gave rise to neurons and glial cells. Here we show that within 10 days of culture, neurospheres contained precursors and differentiated progeny of all three major central nervous system (CNS) cell lineages and these occupied distinct zones. The microenvironment of the inner zone supported cell differentiation. Cells of oligodendroglial lineage generated within the neurosphere were frequently observed. Of these cells, A2B5(+) cells were homogeneously distributed in the neurospheres, NG2(+) cells preferentially occupied the outer zone and O4(+) cells were localized at the inner zone of 10 day-old neurospheres. We prevented a massive cell death of dissociated neurosphere cells seen after differentiation triggered with adhesion and fetal calf serum by adding epidermal growth factor and basic fibroblast growth factor to the culture medium. Under these conditions, less than one third of cells did not express cell specific markers, glial fibrillary acidic protein-positive astroglia represented 43.4%, NG2(+) and/or O4(+) oligodendroglia represented 24.3%, and betaIII-tubulin(+) neurons 3.1% of cells recovered after neurosphere differentiation. We present evidence that oligodendroglial cells differentiate in a stepwise process as a result of their distribution in subsets that represent distinct developmental stages according to antigenic and morphological criteria. These include oligodendrocyte progenitors, preoligodendrocytes, and oligodendrocytes. The highly complex morphology of mature oligodendrocytes was compatible with functional cells.

• MeSH
• antigeny metabolismus   MeSH
• astrocyty fyziologie   metabolismus   MeSH
• buněčná diferenciace MeSH
• buněčné sféroidy MeSH
• fenotyp MeSH
• financování organizované MeSH
• gliový fibrilární kyselý protein metabolismus   MeSH
• inbrední kmeny myší MeSH
• kultivované buňky MeSH
• myši MeSH
• oligodendroglie fyziologie   metabolismus   MeSH
• proteoglykany metabolismus   MeSH
• tubulin metabolismus   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH

We described three different conditions that induce differentiation of dissociated neural stem cells derived from mouse embryonic CNS. In the first set of experiments, where the cell differentiation was triggered by cell adhesion, removal of growth factors and serum-supplemented medium, only sporadic neuronal and astroglial cells survived longer than two weeks and the latter formed a monolayer. When differentiation was induced in serum-free medium supplemented with retinoic acid, rapid and massive cell death occurred. A prolonged survival was observed in cultivation medium supplemented with serum and growth factors EGF plus FGF-2. One third of the cells did not express cell differentiation markers and were responsible for an increase in cell numbers. The remaining cells differentiated and formed the astrocytic monolayer on which occasional neuronal cells grew. One third of the differentiated phenotypes were represented by cells of oligodendroglial lineage. Differentiation of oligodendroglial cells occurred in a stepwise mechanism because the culture contained all successive developmental stages, including oligodendrocyte progenitors, preoligodendrocytes and immature and mature oligodendrocytes. Maturing oligodendrocytes displayed immunocytochemical and morphological features characteristic of cells that undergo physiological development. The cultivation conditions that supported growth and differentiation of neural stem cells were optimal for in vitro developmental studies and the production of oligodendroglial cells.

• MeSH
• apoptóza genetika   MeSH
• buněčná diferenciace fyziologie   MeSH
• fenotyp MeSH
• financování vládou MeSH
• fluorescenční mikroskopie metody   využití   MeSH
• kmenové buňky cytologie   fyziologie   MeSH
• myši anatomie a histologie   MeSH
• oligodendroglie cytologie   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• myši anatomie a histologie   MeSH
• zvířata MeSH
• Publikační typ
• srovnávací studie MeSH

GFP labeled/NE-4C neural progenitor cells cloned from primary neuroectodermal cultures of p53- mouse embryos give rise to neurons when exposed to retinoic acid in vitro. To study their survival and differentiation in vivo, cells were transplanted into the cortex of 6-week-old rats, 1 week after the induction of a photochemical lesion or into noninjured cortex. The electrophysiological properties of GFP/NE-4C cells were studied in vitro (8-10 days after differentiation induction) and 4 weeks after transplantation using the whole-cell patch-clamp technique, and immunohistochemical analyses were carried out. After transplantation into a photochemical lesion, a large number of cells survived, some of which expressed the astrocytic marker GFAP. GFP/GFAP-positive cells, with an average resting membrane potential (Vrest) of -71.9 mV, displayed passive time- and voltage-independent K+ currents and, additionally, voltage-dependent A-type K+ currents (KA) and/or delayed outwardly rectifying K+ currents (KDR). Numerous GFP-positive cells expressed NeuN, betaIII-tubulin, or 68 kD neurofilaments. GFP/betaIII-tubulin-positive cells, with an average Vrest of -61.6 mV, were characterized by the expression of KA and KDR currents and tetrodotoxin-sensitive Na+ currents. GFP/NE-4C cells also gave rise to oligodendrocytes, based on the detection of oligodendrocyte-specific markers. Our results indicate that GFP/NE-4C neural progenitors transplanted into the site of a photochemical lesion give rise to neurons and astrocytes with membrane properties comparable to those transplanted into noninjured cortex. Therefore, GFP/NE-4C cells provide a suitable model for studying neuro- and gliogenesis in vivo. Further, our results suggest that embryonic neuroectodermal progenitor cells may hold considerable promise for the repair of ischemic brain lesions.

• MeSH
• astrocyty fyziologie   MeSH
• buněčná diferenciace účinky léků   MeSH
• buněčné linie MeSH
• denervace metody   MeSH
• ektoderm cytologie   MeSH
• financování organizované MeSH
• fotosenzibilizující látky MeSH
• imunohistochemie MeSH
• ischemie mozku patologie   terapie   MeSH
• kmenové buňky cytologie   fyziologie   MeSH
• membránové potenciály MeSH
• metoda terčíkového zámku MeSH
• modely nemocí na zvířatech MeSH
• mozková kůra fyziologie   chirurgie   patologie   MeSH
• myši MeSH
• neurony cytologie   fyziologie   MeSH
• oligodendroglie fyziologie   MeSH
• přežívání štěpu MeSH
• protinádorové látky farmakologie   MeSH
• transplantace kmenových buněk MeSH
• tretinoin farmakologie   MeSH
• zelené fluorescenční proteiny genetika   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH

• MeSH
• astrocyty fyziologie   MeSH
• axony fyziologie   MeSH
• lidé MeSH
• mozek abnormality   anatomie a histologie   fyziologie   MeSH
• neuroglie MeSH
• neurony fyziologie   MeSH
• oligodendroglie fyziologie   MeSH
• roztroušená skleróza etiologie   patofyziologie   terapie   MeSH
• Schwannovy buňky fyziologie   MeSH
• synapse fyziologie   MeSH
• Check Tag
• lidé MeSH

• MeSH
• demyelinizační nemoci terapie   MeSH
• finanční podpora výzkumu jako téma MeSH
• lidé MeSH
• oligodendroglie cytologie   fyziologie   MeSH
• roztroušená skleróza epidemiologie   patofyziologie   terapie   MeSH
• růstové látky fyziologie   klasifikace   MeSH
• transplantace kmenových buněk metody   využití   MeSH
• Check Tag
• lidé MeSH