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  • 1
    ISSN: 1432-2307
    Keywords: Key words Rat-fibrosarcoma-derived transplantable tumour ; Rat fibrosarcoma-derived cell line ; Myofibroblastic cell ; Histiocytic cell ; Phenotypic modulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A transplantable tumour line (SS) was established in syngeneic rats from a spontaneous fibrosarcoma that had arisen in the submandibular salivary gland of a 24-month-old male F344 rat. A cell line (SS-P) was induced from SS, and a cloned cell line (SS-A3-1) was isolated from SS-P. The primary tumour consisted of oval to spindle-shaped cells arranged in bundles with abundant collagen fibres; ultrastructurally, neoplastic cells exhibited fusiform morphology with prominent rough endoplasmic reticulum. SS tumours showed marked interlacing fascicle and herring-bone growth patterns. SS-P and SS-A3-1 were simmilar morphologically to each other, consisting of oval, spindle or polygonal cells and occasional multinucleated giant cells. Tumours induced by SS-P and SS-A3-1 were histologically similar to SS tumours. Immunohistochemically, all cells in the primary tumour, SS tumours and tumours induced both by SS-P and SS-A3-1 and by SS-P and SS-A3-1 cultures gave a positive reaction to vimentin. Interestingly, neoplastic cells reacting to ED1 (rat macrophage/histiocyte-specific antibody) and α-smooth muscle actin (α-SMA) appeared in SS tumours and tumours induced by SS-P and SS-A3-1 and by SS-P and SS-A3-1 cultures. Cells with histiocytic fine structures and myofibroblastic cells with cytoplasmic actin-like microfilaments were also observed by electron microscopy. The present rat fibrosarcoma-derived transplantable tumour line (SS) and cell lines (SS-P and SS-A3-1) might express myofibroblastic and histiocytic phenotypes, probably depending on the surrounding conditions. These cell lines may prove useful for studying the mechanisms of phenotypic plasticity in neoplastic fibroblasts.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Bergmann glia ; Cerebellar dysplasia ; Immunohistochemistry ; Mutant rat ; Walker’s lissencephaly
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hereditary cerebellar vermis defect (CVD) rats, a new neurological mutant, developed both cerebellar vermis defect and cerebellar dysplasia. Developmental alterations in the cerebellum of the CVD rats were studied chronologically and immunohistochemically. The earliest architectural abnormality was a maldevelopment of the inferior cerebellar peduncle from embryonic day 17 (E17), leading to an indistinct separation between the cerebellum and the pons. From E19, the CVD rats lacked vermis development and, therefore, the cerebellar hemispheres were fused. After birth, Purkinje cells and external granule cells (EGCs) penetrated into the pontine tissue, but retained their normal position until postnatal day 10. Cerebellar lamination began to be disturbed due to abnormal perivascular aggregations of the EGCs, resulting in convoluted and occasionally perivascular lamination. There were no Bergmann glia in the heterotopic cerebellum of the pons, and abnormally arranged Bergmann glia were observed in the mildly disorganized cerebellar hemispheres. Immunohistochemistry for calbindin revealed that abnormal orientation of the Purkinje cells might be related to the perivascular EGCs. Parvalbumin-immunopositive microneurons were seen only in the disarranged molecular layers, and synaptophysin-immunopositive cerebellar glomeruli were present in the afflicted internal granular layers. These findings suggest that perivascular EGCs may play an important role in cerebellar dysplasia and the developmental plasticity in the altered cerebellogenesis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Cell lines ; Rat malignant meningioma ; Morphological heterogeneity ; Nerve growth factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A cell line (KMY-J) was established from a transplantable tumor (MM-KMY) derived from a spontaneous malignant meningioma arising in an aged F344 rat, and three cloned cell lines (KMY-1, KMY-2 and KMY-3) were induced from the parent KMY-J. Morphologically, KMY-J and tumors induced in syngeneic rats by KMY-J showed cell pleomorphism. All neoplastic cells in KMY-J and its tumors were immunoreactive to vimentin; occasional cells reacted to ED1 (rat macrophage/histiocyte-specific antibody) and α-smooth muscle actin (α-SMA), indicating expression of histiocytic or myofibroblastic immunophenotypes of meningioma cells. In contrast, KMY-1, KMY-2 and KMY-3 consisted of a uniform cell population differing from each other. KMY-1-induced tumors were similar histologically to meningeal fibrosarcomas. Dendritic cells seen in KMY-2 cultures gave an appearance of arachnoid trabecular cells. In KMY-3 and its tumors, large round cells and multinucleated giant cells were predominant. Cells of these cloned cell lines also reacted to vimentin, but were negative for ED1 and α-SMA. By the bioassay using PC12 cells and reverse transcription-polymerase chain reaction for nerve growth factor (NGF) mRNA, production of NGF was demonstrated in the parent and cloned cell lines. The present cell lines may prove useful for studying the histological features of meningeal tumors and the bioactive factors produced by meningeal cells.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Key words Cerebellar dysplasia ; Medullomyoblastoma ; Primitive neuroectodermal tumor ; Ethyl-nitrosourea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 26-week-old female cerebellar vermis defect (CVD) rat, a mutant with cerebellar vermis defect and cerebellar dysplasia, developed a brain tumor about 10 mm in diameter. Histopathologically, the tumor consisted of diffuse proliferation of small round to ovoid cells with hyperchromatic nuclei, occasionally containing round to strap-shaped myoblastic cells. Immunohistochemically, the small round cells expressed neuron-specific enolase and synaptophysin, indicating neuronal differentiation; myoblastic components reacted to desmin, myoglobin, and vimentin. Based on these findings, the case was diagnosed as a medullomyoblastoma (MMB). Furthermore, two cerebella tumors in CVD rats, which were induced by transplacental application of ethyl-nitrosourea, showed histopathology similar to the aforementioned case. MMB is a very rare tumor in humans and animals; thus, it is noteworthy that MMBs developed in CVD rats, involving the dysplastic cerebellum with abnormal migration of external granule cells.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0533
    Keywords: Key words Bergmann glia ; Cell migration ; Cerebellar ¶dysplasia ; Immunohistochemistry ; Mutant rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cerebellar vermis defect (CVD) rat is a new neurological mutant characterized by a cerebellar vermis defect and dysplasia in the cerebellum, especially at the cerebellopontine junctions. In this study, the cytokinetics of glia in terms of the development of cerebellar dysplasia in the CVD rat was investigated using glial fibrillary acidic protein (GFAP) and vimentin immunohistochemistry. In the cerebellar hemispheres, dislocation of the Bergmann glia was observed from postnatal day 5 (P5) in lesions with abnormally aggregated external granule cells (EGCs). Rearranging Bergmann glia were often seen around the EGCs penetrating into the white matter. In the cerebellopontine junctional areas, Bergmann glia were induced after penetration of the Purkinje cells, identified with calbindin immunohistochemistry, and EGCs into the pons from P10. Bergmann fibers were frequently arranged perivascularly. In the clusters of Purkinje cells without EGC settlement in the pons, a small number of Bergmann fibers were observed and their alignment was completely disturbed. These findings suggest that morphological changes in the Bergmann glia depend on their contact with Purkinje cells, but that the orientation of their processes may be influenced by EGC settlement. These glial fibers in the CVD rat may play an important role in the aberrant migration of EGCs, resulting in the development of cerebellar dysplasia.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0533
    Keywords: Key words Bromodeoxyuridine ; Cerebellar dysplasia ; Migration disorder ; Mutant rat ; Walker’s lissencephaly
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hereditary cerebellar vermis defect rat (CVD) is a new neurological mutant characterized by cerebellar vermis defect and a dysplastic cerebellum, especially in the cerebello-pontine junctions. In this study, the cytokinetics of neuronal migrations in the CVD were analyzed using 5-bromo-2′-deoxyuridine (BrdU) as a labeling marker. From embryonic day 21, the CVD cerebellum was small in size with retarded foliation, but no significant differences were detected in the migration pattern of the BrdU-labeled cells between the unaffected controls and the CVD during the prenatal period. On postnatal day 0 (P0), heterotopic Purkinje cells, demonstrable by calbindin immunohistochemistry, were seen in the dorsal pons of the CVD. From P4, BrdU-positive external granule cells (EGCs), which were labeled by BrdU injection on P2, began to penetrate the pons. From P5, the EGCs aggregated around the blood vessels, leading to a disturbance of the cerebellar lamination both in the cerebello-pontine junctions and in the cerebellar hemispheres. Thereafter, the BrdU-labeled cells in the perivascularly aggregated EGCs migrated radially, and formed internal granular layers around the vessels, indicating an aberrant perivascular migration of the EGCs. These findings suggest that the EGC dislocation was preceded by an aberrant settlement of the Purkinje cells, and that the perivascularly aggregated EGCs resulted in cerebellar dysplasia in the CVD.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Apoptosis, a mechanism for removal of genetically damaged cells and for maintenance of desired size of cell populations, has been implicated in tumor development. Previously, we defined polymorphic loci for susceptibility to apoptosis of thymocytes Rapop1, Rapop2, and Rapop3 on mouse Chromosomes 16, 9, and 3, respectively, using recombinant congenic CcS/Dem strains, each of which contains a random set of 12.5% STS/A genome in the genetic background of BALB/cHeA. The STS/A alleles at these loci confer lower susceptibility to radiation-induced apoptosis of thymocytes than the BALB/cHeA. In the present study, we tested susceptibility of colon crypt cells to radiation-induced apoptosis. In contrast to apoptosis in thymus, the STS/A mice were more susceptible to apoptosis in colon than the BALB/cHeA. Among the CcS/Dem strains, CcS-4, CcS-7, and CcS-16 were more susceptible to apoptosis in colon than the BALB/cHeA; in thymus, the CcS-7 mice are less susceptible, and the CcS-4 and CcS-16 are not different from the BALB/cHeA. Thus, individual CcS/Dem strains showed different apoptosis susceptibility in the two organs. Analysis of (CcS-7 × BALB/cHeA)F2 hybrids revealed linkage of susceptibility to radiation-induced apoptosis of colon crypt cells to two loci on Chrs 9 and 16, to which Rapop2 and Rapop1 are mapped. The STS/A allele at the locus on chromosome 9 results in high susceptibility to apoptosis of colon crypt cells in mice homozygous for the BALB/cHeA allele at the locus on Chr 16. Although these two loci may be identical to Rapop1 and Rapop2, they affect apoptosis in colon in a way different from that in thymus.
    Type of Medium: Electronic Resource
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