摘要:

AbstractNumerous studies of the past decade have illuminated the importance of intercellular adhesion events for neural pattern formation. It has been documented that members of the Ig and cadherin gene superfamilies, that glycoproteins and, probably to some extent, proteoglycans of the extracellular matrix play a role in this context. Recent observations suggest that, in addition to adhesive interactions, repulsive and/or inhibitory phenoma are also of importance in regulating neural pattern formation. Several molecules are under study which are cosidered possible mediators of inhibitory interactions in the nervous system. The hypothesis has been advanced that some of these might be partially responsible for restrictive, boundary‐like properties ascribed to glial cells in developing and regenerating tissues. The current review summarizes these studies and focusses on molecular aspects of boundary and compartmentation phenomena. © 1995 Wiley‐Liss,

ISSN:0894-1491    

DOI:10.1002/glia.440130402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractAssessment of glial cell behaviour during optic nerve (ON) regeneration inXenopustadpoles is hampered by the lack of classical cellular markers that distinguish different glial cells in mammals. We thus have characterized the intermediate filament (IF) complement of tadpole glial cells and used it to follow the fate of glial cell subsets during the first 10 days after ON crush. Glial cells synthesize a restricted number of cytokeratin (CK) species and vimentin. This pattern remains essentially unchanged during metamorphosis and regeneration. However, vimentin turnover is specifically enhanced after injury. The expression of CKs and vimentin has been followed immunocytochemically in situ and in isolated cells recovered from dissociated ON segments. In the normal nerve, 79% of ramified glial cells express both CK and vimentin, 1% CK and 4% vimentin only, whereas 16% express neither IF protein. We tentatively classified CK expressing cells as mature astrocytes and those without IF proteins as oligodendrocytes. In the regenerating ON, the relative number of oligodendrocytes is decreased, while the astrocytic subset becomes accordingly larger but is decreased by day 10 already in favour of cells expressing vimentin only. Astrocytes invade the lesion site soon after crush, arrange into a central core within the distal nerve segment and establish a peripheral scaffold that is readily crossed by axons. Unlike mammalian astrocytes that remain absent from the lesion site but form a scar at some distance to it, amphibian astrocytes appear to provide active guidance to axons growing through the lesion site. © 1995 Wiley‐Liss, I

ISSN:0894-1491    

DOI:10.1002/glia.440130403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractGlial‐like cells in rat pituitary intermediate lobe were localized and characterized by immunohistochemistry with antisera against glial fibrillary acidic protein (GFAP) and S‐100. Individual GFAP immunoreactive (IR) cells possessed several processes that often branched into secondary and tertiary processes, terminating with end‐feet. The GFAP‐immunopositive cell population was distributed in specific rostrocaudal and dorsoventral patterns. The distribution and numbers of cells differed between male and female rats. Examination of altered physiological states, e.g., adrenalectomy, lactation, and salt‐loading, revealed state‐specific changes in the appearance and distribution of GFAP‐IR cells. Adrenalectomy and lactation increased GFAP‐IR glial‐like cell numbers, whereas salt‐loading decreased their numbers and the typical pattern of distribution. By contrast, S‐100–expressing cells were evenly distributed in male and female rats, and its expression was not affected by the experimental conditions. Double‐label immunocytochemistry indicated that GFAP‐IR cells are a subpopulation of S‐100‐IR cells. These results suggest that cells normally expressing only S‐100 may be induced to express GFAP under altered physiologic cond

ISSN:0894-1491    

DOI:10.1002/glia.440130404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractWe have previously shown that long‐term treatment of primary cultured astrocytes with TGFβ1 induces morphological changes accompanied by increases in actin and GFAP synthesis, and a profound rearrangement of the cytoskeleton. The present report describes the short‐term reorganization of actin filaments induced by TGFβ1 in rat cerebellum cultured astrocytes and in an astrocytic cell line. TGFβ1 caused the appearance of new actin and vinculin organizations, without protein synthesis. This cytoskeletal rearrangement was followed by altered cell‐cell interactions. All these changes induced by TGFβ1 were different and slower than those induced by serum, PDGF, and endothelin. TGFβ1 induced the appearance of lamellipodia, organelles found at the cell front of motile cells in low‐density cultures of immortalized astrocytes. These results indicate that the changes in the astrocyte cytoskeleton induced by TGFβ1 are probably associated with cell movement. The events promoted by TGFβ1 might help to clarify its action in the brain during embryogenesis and in tissue repair. Copy 1995 W

ISSN:0894-1491    

DOI:10.1002/glia.440130405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractMonoclonal antibodies (mAbs) against the major constituents of cartilage extracellular matrix, aggrecan and link protein, were screened by indirect immunofluorescence on frozen sections of bovine spinal cord. Antibodies against aggrecan and link protein gave rise to very similar perineuronal labeling in spinal cord gray matter. Aggrecan and link protein reactivities were seen in other regions of the central nervous system (CNS), although their distributions were not always coincident. Pretreatment of the tissue section withStreptomyceshyaluronidase, which is hyaluronate‐specific, led to the loss of both reactivities. On Western blots, anti‐aggrecan mAbs reacted with a large chondroitin sulfate proteoglycan. The chondroitinase‐treated CNS proteoglycan co‐migrated with the chondroitinase‐ and keratanase‐treated cartilage proteoglycan. In CNS tissue homogenates, the addition ofStreptomyceshyaluronidase brought about the release of the proteoglycan from the tissue. Anti‐link protein mAbs were reactive with two species in the bovine CNS, the mobilities of which were very similar to those of the cartilage link proteins. The release of these species from the tissue required hyaluronidase. A rabbit antiserum against aggrecan was used to identify a similar proteoglycan in the rat CNS. In spinal cord‐derived cell cultures, the labeled material was associated with astrocytes. An aggrecan cDNA hybridized to a 9.5 kb mRNA in the rat CNS. We conclude that the perineuronal matrix consists, in part, of a hyaluronate‐bound aggrecan‐like proteoglycan and link proteins, and that the former is produced by astrocytes. ©

ISSN:0894-1491    

DOI:10.1002/glia.440130406

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractMechanisms regulating Schwann cell proliferation during development are unclear. Schwann cell division is known to be driven by an unidentified mitogen present on the surface of axons, but it is not known whether other molecules play a role in regulating this proliferation. Transforming growth factor‐beta (TGF‐β) which is found in the developing peripheral nervous system (PNS) and is mitogenic for neuron‐free Schwann cells in vitro could be involved. We have investigated the effects of TGF‐β 1, TGF‐β 2 and antibodies to TGF‐β and TGF‐β 2 on axon driven Schwann cell proliferation. Rat embryonic dorsal root ganglion neurons (DRG) neurons and Schwann cells from the sciatic nerve were isolated, purified and recombined in vitro. Confirming earlier reports by others, we observed that TGF‐β 1 and TGF‐β 2 added to the culture medium stimulated the proliferation of Schwann cells in the absence of neurons. However, when added to neuron‐Schwann cell co‐cultures, TGFβ caused a variable response ranging from no effect to moderate inhibition of Schwann cell proliferation in different experiments. A stimulation of Schwann cell proliferation by TGFβ was never observed in neuron‐Schwann cell co‐cultures. Antibodies to TGF‐β and TGF‐β 2 did not influence axon driven Schwann cell proliferation. To further determine the role of TGF‐β in Schwann cell proliferation and myelination, we studied Schwann cell proliferation in cultures from mice in which the TGF‐β 1 gene was delected by homologous recombination. Neuron‐Schwann cell cultures from wild‐type, heterozygous and homozygous mice were used. No differences were observed in either Schwann cell proliferation or myelination between cultures obtained from homozygous mutants and their heterozygous and wild‐type controls. These findings suggest that TGF‐β does not function as a part of the mitogenic mechanism presented by neurons to Schwann cells, but that the presence of active TGFβ in the cellular environment might regulate the degree of proliferatio

ISSN:0894-1491    

DOI:10.1002/glia.440130407

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractNeuroepithelial progenitor cells from forebrains of newborn rat pups develop into “mature” astrocytes in an epidermal growth factor‐containing medium free of serum (Von Visger et al: Exp Neurol 128:34, 1994). Eight‐week‐old “mature” astrocyte cultures on poly‐L‐lysine‐coated dishes were exposed to an acidic medium (pH 5.8–6.0) for 2–6 h. Immunoreactivity for glial fibrillary acidic protein (GFAP) dramatically and rapidly increased; this immediate increase was not affected by pretreatment with cycloheximide. In further experiments we found that the increase in GFAP was undiminished for 24–48 h after the acid‐treated astrocytes were returned to normal growth medium. The Ca2+channel antagonists nifedipine and diltiazemattenuatedthe increase in GFAP immunoreactivity. These results suggest that extracellular acidosis may produce a rapid increase in GFAP immunoreactivity in astrocytes independent of de novo protein synthesis, possibly by increasing intracellular levels of free Ca2+ions

ISSN:0894-1491    

DOI:10.1002/glia.440130408

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0894-1491    

DOI:10.1002/glia.440130401

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY