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Biomedical subjects

G Sobue

Publications and source records attributed to G Sobue.

At least 325 records · Page 18Linked to original sources
PubMed1987

Size-dependent myelinated fiber loss in the corticospinal tract in Shy-Drager syndrome and amyotrophic lateral sclerosis.

Morphometric evaluation was performed on myelinated fibers of the corticospinal tract at the seventh thoracic spinal cord segment from three patients with Shy-Drager syndrome (SDS), six patients with amyotrophic lateral sclerosis (ALS), and five patients with nonneurologic symptoms. In SDS, small-sized myelinated fibers were nearly completely depleted, while large-sized myelinated fibers were considerably well preserved. In ALS, on the contrary, large myelinated fibers were predominantly decreased. These results suggested that selective vulnerability of axonal loss depends on fiber size and should be considered in interpretation of pathology of corticospinal tracts.

Amyotrophic Lateral Sclerosis↗
PubMed1986

Schwann cell galactocerebroside of unmyelinated fibers is inducible by derivatives of adenosine 3',5'-monophosphate.

By using indirect immunofluorescence, galactocerebroside (galC) was detected on the surface of Schwann cells cultured from unmyelinated fibers of 10- to 12-day-old rat cervical sympathetic nerve trunk. By day 4 in vitro, galC-positive cells disappeared from the culture. When the 4-day cultures were treated with 1 mM 8-bromo cyclic AMP or dibutyryl cyclic AMP, galC reappeared in 72 h. The proportion of Schwann cells expressing galC was dependent on the concentration of cyclic AMP derivatives used.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1986

Schwann cell responses to cyclic AMP: proliferation, change in shape, and appearance of surface galactocerebroside.

Surface galactocerebroside (galC) was induced on cultured Schwann cells by two analogues of cyclic adenosine 3',5'-monophosphate (cAMP), dibutyryl cAMP and 8-bromo cAMP (as previously reported by Sobue and Pleasure) and also by forskolin, a potent adenylate cyclase activator. These reagents also induced a morphological transition of many of the Schwann cells, from an elongated spindle shape to flattened cells extending fenestrated cytoplasmic sheets. Surface galC and these changes in Schwann cell shape were not elicited by raising the extracellular cAMP concentration, nor by many compounds known to promote the differentiation of other cell types, suggesting that intracellular cAMP is the unique signal for their induction. The cAMP analogues also induced Schwann cell proliferation (as previously reported by Raff et al.), as did forskolin. The concentrations of cAMP analogues and forskolin eliciting largest increases in numbers of Schwann cells in the cultures were 10-fold lower than the concentrations required for optimal induction of Schwann cell surface galC.

Animals↗
PubMed1986

Peripheral nerve involvement in familial chorea-acanthocytosis.

Myelinated fibers and neuronal cell bodies of the ventral spinal outflow and primary sensory neurons were histopathologically examined in a patient with familial chorea-acanthocytosis and age-matched controls. The patient exhibited a marked loss of large myelinated axons and their neuronal cell bodies in the ventral spinal outflow, while there was frequent occurrence of axonal sprouts. Large myelinated fibers in sensory afferents were also decreased in number. Segmental de- and remyelination was markedly increased in teased fiber preparations of both motor and sensory peripheral nerves.

Acanthocytes↗
PubMed1986

Schwann-like cells cultured from human dermal neurofibromas. Immunohistological identification and response to Schwann cell mitogens.

Primary cultures prepared from dermal and plexiform neurofibromas contain Schwann-like cells and fibroblast-like cells. SLC are elongated and bipolar or multipolar. By indirect immunofluorescence light microscopy, living SLC bind antibodies against laminin and against nerve growth factor receptor to their surface, but not antibodies against fibronectin. In these respects, cultured SLC are indistinguishable from cultured human adult Schwann cells. FLC are flat and pleomorphic. By indirect immunofluorescence light microscopy, living FLC bind antibodies against fibronectin but not against laminin or NGFR. In these respects, cultured FLC are indistinguishable from cultured human adult endoneurial fibroblasts. Considerable purification of viable SLC from SLC/FLC mixed cultures can be achieved by flow cytofluorometry using a monoclonal anti-NGFR antibody. Tritiated thymidine radioautography indicated that mitosis of SLC in mixed SLC/FLC cultures prepared from dermal neurofibromas is infrequent in MEM with 10% calf serum, more frequent in RPMI 1640 medium with 15% fetal calf serum. Central nervous system axolemmal fragments (rat or human) elicited a greater than 10-fold SLC proliferative response in mixed SLC/FLC cultures from three of seven dermal neurofibromas (from six patients with neurofibromatosis), but had no effect on SLC mitosis in cultures from the other four dermal neurofibromas. SLC mitosis was inhibited by concentrations of cyclic adenosine 3',5'-monophosphate analogues known to stimulate proliferation of normal rat Schwann cells. Glial growth factor partially purified from bovine pituitaries stimulated SLC mitosis both in SLC/FLC mixed cultures and in cultures of purified SLC. The studies we have described indicate that neurofibroma SLC can be cultured, unequivocally identified in culture by morphological and immunohistological criteria, purified, and stimulated to proliferate by several Schwann cell mitogens. Further quantitative comparisons of the baseline and mitogen-stimulated rates of proliferation of SLC and age-matched control human Schwann cells are needed, however, to determine which of the two alternate pathogenetic mechanisms for formation of neurofibromas mentioned in the introduction is correct.

Axons↗
PubMed1986

Shy-Drager syndrome: neuronal loss depends on size, function, and topography in ventral spinal outflow.

We analyzed myelinated fibers and neurocytons in the ventral spinal outflow of patients with Shy-Drager syndrome. Axonal loss occurred predominantly in thin, myelinated fibers that correspond mainly to autonomic preganglionic axons. Intermediate and large myelinated fibers, mainly gamma and alpha axons, were also involved, but to a lesser degree. Neuronal and axonal loss was more prominent in caudal segments and less in rostral segments. Axonal degeneration in single teased fibers was seen frequently in ventral spinal roots.

Aged↗
PubMed1986

Nerve growth factor receptors on dissociated neurofibroma Schwann-like cells.

Neurofibromatosis is a disorder which predominantly involves cellular elements of peripheral neural sheaths. Little is known about the regulation of differentiation and proliferation of cells comprising neurofibromas. Because nerve growth factor-like activity may be present in neurofibromas and the cells comprising neurofibromas are neural crest derivatives, we have investigated whether nerve growth factor (NGF) receptors are present on cells from dissociated dermal neurofibromas. Using 125I-NGF to measure binding to cultured cells in suspension and for autoradiography, we identified a population of cells having characteristics of Schwann cells which exhibited saturable 125I-NGF binding. This binding is characteristic of the "fast" (low affinity) NGF receptor, having a Kd of approximately 1 nM and a Bmax of at least 120 fmol/10(6) cells. Less than 20% of the bound 125I-NGF (5 ng/ml) is not displaced when transferred to 0 degrees C by an excess of unlabeled NGF (10 micrograms/ml) and is therefore bound to either "slow" (high affinity) sites or is rapidly internalized. NGF receptors with characteristics of fast sites have recently been reported on Schwann-like cells from chick dorsal root ganglia [Zimmerman, A., and Sutter, A. Beta nerve growth factor (beta NGF) receptors on glial cells. Cell-cell interaction between neurones and Schwann cells in culture of chick sensory ganglia. EMBO J., 2: 879-885, 1983]. The identification of NGF receptors on both fetal chick dorsal root ganglia and neurofibroma Schwann-like cells suggests that NGF may have a role in the regulation of Schwann cell function in both normal development and in neurofibromatosis.

Cells, Cultured↗
PubMed1985

Products of activated lymphocytes stimulate Schwann cell mitosis in vitro.

Culture of Schwann cells and endoneurial fibroblasts from newborn rat sciatic nerves in the presence of supernatants obtained from concanavalin A (Con-A)-stimulated rat mononuclear cells resulted in proliferation of both cell types. Con-A did not induce Schwann cell or fibroblast proliferation. Supernatant from a Gibbon T-cell lymphoma and chromatographically purified rat interleukin-2 (IL-2) induced fibroblast but not Schwann cell proliferation, and cloned human IL-2 did not induce proliferation of either cell type. Proliferation of Schwann cells and endoneurial fibroblasts induced by activated mononuclear inflammatory cells may be important in inflammatory demyelinative neuropathies.

Animals↗
PubMed1985

Experimental lead neuropathy: inorganic lead inhibits proliferation but not differentiation of Schwann cells.

Schwann cells were prepared from the sciatic nerves of newborn rats and cultured in a monolayer. Addition of lead acetate at concentrations between 0.4 and 10.0 micrograms/ml, levels comparable to those occurring in neural tissues and physiological fluids of lead-intoxicated rats, diminished both the baseline rate of proliferation of the Schwann cells and their response to the mitogens, axolemmal fragments, glial growth factor, and the adenosine 3':5'-cyclic monophosphate (cAMP) analogues 8-bromo-cAMP and dibutyryl-cAMP. This demonstrates a direct toxic effect of inorganic lead on Schwann cells. Lead acetate in this concentration range did not, however, inhibit the cAMP analogue-induced appearance of the "myelin marker" lipid galactocerebroside on the surfaces of the cultured Schwann cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

Tissue culture studies of neurofibromatosis: effects of axolemmal fragments and cyclic adenosine 3',5'-monophosphate analogues on proliferation of Schwann-like and fibroblast-like neurofibroma cells.

Six dermal neurofibromas obtained from 5 patients with neurofibromatosis were dissociated and the cells were plated on polylysine-coated glass. Two principal cell types were observed in the cultures: elongated and bipolar Schwann-like cells (SLCs), and polymorphic flattened fibroblast-like cells (FLCs). Indirect immunofluorescence demonstrated that SLCs expressed surface laminin but not surface fibronectin; FLCs expressed surface fibronectin but were only weakly positive for surface laminin. Tritiated thymidine autoradiography demonstrated that cultured SLCs proliferated slowly (labeling index, 0.7 to 4.0%), whereas FLCs divided more rapidly (labeling index, 7.5 to 26.4%). Axolemmal fragments prepared from human or rat central nervous system specimens adhered to SLCs derived from each of the 6 neurofibromas, but not to FLCs. Axolemmal fragments induced a marked proliferative response of SLCs from 2 of the 6 neurofibromas but had no effect on proliferation of SLCs from the other 4 neurofibromas or FLCs from any of the 6 neurofibromas. In one patient from whom 2 neurofibromas were obtained, SLCs from one neurofibroma responded to axolemmal fragments, while SLCs from the other did not. Treatment of the cultures with 0.1 mM cyclic adenosine 3'5'-monophosphate (cAMP) analogue, 8-bromo cAMP, caused marked inhibition of proliferation of both SLCs and FLCs derived from all 6 neurofibromas. The same concentration of another cAMP analogue, dibutyryl cAMP, inhibited proliferation of SLCs but not of FLCs.

Adult↗