| 1. |
- Blixt Wojciechowski, Anita, et al.
(författare)
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Migratory capacity of the cell line RN33B and the host glial cell response after subretinal transplantation to normal adult rats
- 2004
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Ingår i: Glia. - : John Wiley & Sons. - 0894-1491 .- 1098-1136. ; 47:1, s. 58-67
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Tidskriftsartikel (refereegranskat)abstract
- As previously reported, the brain-derived precursor cell line RN33B has a great capacity to migrate when transplanted to adult brain or retina. This cell line is immortalized with the SV40 large T-antigen and carries the reporter gene LacZ and the green fluorescent protein GFP. In the present study, the precursor cells were transplanted to the subretinal space of adult rats and investigated early after grafting. The purpose was to demonstrate the migration of the grafted cells from the subretinal space into the retina and the glial cell response of the host retina. Detachment caused by the transplantation method was persistent up to 4 days after transplantation, and then reattachment occurred. The grafted cells were shown to migrate in between the photoreceptor cells before entering into the plexiform layers. Molecules involved in migration of immature neuronal cells as the polysialylated neural cell adhesion molecule (PSA-NCAM) and the collapsing response-mediated protein 4 (TUC-4) was found in the plexiform layers of the host retina, but not in the grafted cells. The expression of the intermediate filaments GFAP, vimentin, and nestin was intensely upregulated immediately after transplantation. A less pronounced upregulation was observed on sham-operated animals. In summary, the RN33B cell line migrated promptly posttransplantation and settled preferably into the plexiform layers of the retina, the same layers where the migration cues PSA-NCAM and TUC-4 were established. In addition, both the transplantation method per se and the implanted cells caused an intense glial cell response by the host retina.
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| 2. |
- Forsberg-Nilsson, Karin, et al.
(författare)
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Oligodendrocyte precursor hypercellularity and abnormal retina development in mice overexpressing PDGF-B in myelinating tracts
- 2003
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Ingår i: Glia. - : Wiley. - 0894-1491 .- 1098-1136. ; 41:3, s. 276-89
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Tidskriftsartikel (refereegranskat)abstract
- Platelet-derived growth factor (PDGF) influences the generation of neurons and glia during embryogenesis and in early postnatal life. In an attempt to determine the consequences of an overexpression of PDGF-B during the first weeks of life, we targeted transgenic expression of a human PDGF-B cDNA to myelinating tracts using the promoter region of the myelin basic protein (MBP) gene. Transgenic mRNA and protein were expressed in the brain and the expression profile of the human PDGF-B during early postnatal development closely paralleled that of the endogenous mouse MBP gene. The gross morphological appearance of transgenic brains was normal but at the cellular level several phenotypic alterations could be identified. In white matter tracts such as the corpus callosum and cerebellar medulla, there was a marked hypercellularity. The number of oligodendrocyte precursors was increased and astrocytes were more abundant. In adult mice carrying the MBP-PDGF-B transgene, however, myelination appeared normal and the amount of oligodendrocytes was similar to that of control littermates. In addition to the phenotypic alterations in the brain, investigation of eye structure revealed a striking disorganization of retinal architecture. The retina was folded with cells collected in papillar or follicular-like structures. Retinal whole mount preparations after India ink perfusion revealed capillary disorganization with large-caliber vessels supporting only a few fine branches. Our observations strengthen the notion that PDGF is an important effector molecule in postnatal CNS development.
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| 3. |
- Ghosh, Fredrik, et al.
(författare)
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Müller cells in allogeneic adult rabbit retinal transplants.
- 2002
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Ingår i: GLIA. - : Wiley. - 1098-1136 .- 0894-1491. ; 40:1, s. 78-84
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Tidskriftsartikel (refereegranskat)abstract
- Müller cell morphology and degree of activation in adult retinal transplants have, to our knowledge, never been reported previously. We transplanted adult rabbit neuroretinal full-thickness sheets, prepared under strict control, to the subretinal space of adult rabbits. After surviving 6-174 days, eyes were examined in the light microscope, and grafts displaying the normal laminated morphology were labeled with antibodies against vimentin and glial fibrillary acidic protein (GFAP). Müller cells in the grafts displayed the normal vertical arrangement, from outer limiting membrane to vitread endfeet. They showed an initial degree of activation, evident by GFAP upregulation, which diminished with increasing survival times, and was absent in the oldest specimens. In the host retina, Müller cells in the transplant area became progressively more disorganized with increasing survival times, and their degree of activation increased. Our results suggests that adult full-thickness neuroretinal grafts are structurally stable, even in long-term specimens, and thrive in spite of their allogeneic environment. The gliotic change seen in the host retina covering the graft is identical to the one seen in earlier reported eyes receiving embryonic grafts, and is due to the merangiotic nature of the rabbit neuroretina. GLIA 40:78-84, 2002. Copyright 2002 Wiley-Liss, Inc.
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| 4. |
- Ghosh, Fredrik
(författare)
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Müller cells in long-term full-thickness retinal transplants.
- 2002
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Ingår i: GLIA. - : Wiley. - 1098-1136 .- 0894-1491. ; 37:1, s. 76-82
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Tidskriftsartikel (refereegranskat)abstract
- Müller cells are essential in creating and maintaining intricate neuroretinal architecture. The functions of this important glial cell are not limited to mere support of the retinal neurons, but also include interaction in synaptic transmission and activation in response to retinal insult. In this study, we have examined Müller cell morphology and degree of activation in embryonic full-thickness rabbit neuroretinal grafts, which were positioned under the host retina using vitrectomy technique. After surviving 3-10 months, retinal specimens were examined with hematoxylin and eosin staining and immunohistochemical analysis of vimentin and glial fibrillary acidic protein (GFAP) expression. In the host retina covering the graft, outer layers were degenerated, and vimentin-labeled Müller cells in this area appeared short, disorganized, and displayed strong GFAP labeling. In the graft, vimentin-labeled Müller cells spanning the retinal layers in the normal manner were found. Müller cells in 3-month grafts were well labeled by GFAP, whereas in older grafts, GFAP labeling was very weak or absent. Our results suggest that Müller cells in well-laminated full-thickness retinal grafts display many of the normal morphological features and retain a normal organization even after prolonged survival times. The loss of the initial degree of Müller cell activation indicates a long-term stability of the graft. The degeneration and gliosis of the host retina covering the graft is best explained by the merangiotic nature of the rabbit retina and may limit the usefulness of the rabbit in retinal transplantation experiments.
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