Supraorganized collagen enhances Schwann cell reactivity and organization in vitro

We investigated the reactivity and expression of basal lamina collagen by Schwann cells (SCs) cultivated on a supraorganized bovine-derived collagen substrate. SC cultures were obtained from sciatic nerves of neonatal Sprague-Dawley rats and seeded on 24-well culture plates containing collagen substrate. The homogeneity of the cultures was evaluated with an SC marker antibody (anti-S-100). After 1 week, the cultures were fixed and processed for immunocytochemistry by using antibodies against type IV collagen, S-100 and p75NTR (pan neurotrophin receptor) and for scanning electron microscopy (SEM). Positive labeling with antibodies to the cited molecules was observed, indicating that the collagen substrate stimulates SC alignment and adhesion (collagen IV labeling - organized collagen substrate: 706.33 ± 370.86, non-organized collagen substrate: 744.00 ± 262.09; S-100 labeling - organized collagen: 3809.00 ± 120.28, non-organized collagen: 3026.00 ± 144.63, P < 0.05) and reactivity (p75NTR labeling - organized collagen: 2156.33 ± 561.78, non-organized collagen: 1424.00 ± 405.90, P < 0.05; means ± standard error of the mean in absorbance units). Cell alignment and adhesion to the substrate were confirmed by SEM analysis. The present results indicate that the collagen substrate with an aligned suprastructure, as seen by polarized light microscopy, provides an adequate scaffold for SCs, which in turn may increase the efficiency of the nerve regenerative process after in vivo repair.

Nidogen Plays a Role in the Regenerative Axon Growth of Adult Sensory Neurons Through Schwann Cells

We previously reported that nidogen is an extracellular matrix protein regulating Schwann cell proliferation and migration. Since Schwann cells play a critical role in peripheral nerve regeneration, nidogen may play a role in it via regulation of Schwann cells. Here, we demonstrate direct evidence that nidogen induces elongation of regenerative axon growth of adult sensory neurons, and that the effect is Schwann cell dependent. Continuous infusion of recombinant ectodomain of tumor endothelial marker 7, which specifically blocks nidogen function in Schwann cells, suppressed regenerative neurite growth in a sciatic nerve axotomy model. Taken together, it is likely that nidogen is required for proper regeneration of peripheral nerves after injury.

S100ß and fibroblast growth factor-2 are present in cultured Schwann cells and may exert paracrine actions on the peripheral nerve injury / S100ß e fator de crescimento de fibroblasto-2 estão presentes nas células de Schwann cultivadas e exercem ações parácrinas na lesão do nervo

PURPOSE: The neurotrophic factor fibroblast growth factor-2 (FGF-2, bFGF) and Ca++ binding protein S100ß are expressed by the Schwann cells of the peripheral nerves and by the satellite cells of the dorsal root ganglia (DRG). Recent studies have pointed out the importance of the molecules in the paracrine mechanisms related to neuronal maintenance and plasticity of lesioned motor and sensory peripheral neurons. Moreover, cultured Schwann cells have been employed experimentally in the treatment of central nervous system lesions, in special the spinal cord injury, a procedure that triggers an enhanced sensorymotor function. Those cells have been proposed to repair long gap nerve injury. METHODS: Here we used double labeling immunohistochemistry and Western blot to better characterize in vitro and in vivo the presence of the proteins in the Schwann cells and in the satellite cells of the DRG as well as their regulation in those cells after a crush of the rat sciatic nerve. RESULTS: FGF-2 and S100ß are present in the Schwann cells of the sciatic nerve and in the satellite cells of the DRG. S100ß positive satellite cells showed increased size of the axotomized DRG and possessed elevated amount of FGF-2 immunoreactivity. Reactive satellite cells with increased FGF-2 labeling formed a ring-like structure surrounding DRG neuronal cell bodies.Reactive S100ß positive Schwann cells of proximal stump of axotomized sciatic nerve also expressed higher amounts of FGF-2. CONCLUSION: Reactive peripheral glial cells synthesizing FGF-2 and S100ß may be important in wound repair and restorative events in the lesioned peripheral nerves.

OBJETIVO: O fator neurotrófico fator de crescimento de fibroblastos-2 (FGF-2, bFGF) e a proteína ligante de Ca++ S100ß são expressos pelas células de Schwann dos nervos e por células satélites do gânglio da raiz dorsal (GRD). Estudos recentes indicam a importância das moléculas nos mecanismos parácrinos relacionados à manutenção neuronal e à plasticidade de neurônios periféricos motores e sensoriais. Além disso, células de Schwann cultivadas têm sido empregadas experimentalmente no tratamento de lesões no sistema nervo central, especialmente na lesão da medula espinal, a qual mostrou uma melhora da função sensoriomotora. Estas células são ainda propostas no reparo do nervo lesado com perda de tecido. MÉTODOS: Usamos a dupla marcação imunohistoquímica e o Western blot para caracterizar melhor in vitro e in vivo a presença das proteínas nas células de Schwann e nas células satélites do GRD assim como sua regulação nessas células após a compressão do nervo ciático de ratos. RESULTADOS: FGF-2 e S100ß estão presentes nas células de Schwann do nervo ciático e nas células satélites do GRD. Células satélites do GRD axotomizado positivas para S100ß possuíam quantidade aumentada de imurreatividade da FGF-2. Células satélites reativas apresentando maior quantidade de FGF-2 formaram um anel ao redor dos corpos neuronais do GRD. Células de Schwann do coto proximal à axotomia do nervo ciático e positivas para S100ß também expressaram quantidades aumentadas de FGF-2. CONCLUSÃO: As células gliais periféricas ao sintetizar FGF-2 e S100ß podem ser importantes no reparo de cicatrização e em eventos restaurativos nas lesões do nervo.

Terminal schwann cell distribution at the neuromuscular junction of the dystrophin-deficient MDX mice

The murine model of muscular dystrophy, the mdx mice, is widely used to study the pathogenesis of muscular dystrophies. These mice suffer an X-linked dystrophin deficiency and present cycles of muscle fiber degeneration-regeneration beginning at 21 days of age. At the present, we studied neuromuscular junction organization in the sternomastoid muscle of mdx mice, focusing on the distribution of terminal Schwann cells during early development and adults. Seven and 14 days after birth (n=200 endplates for each age), before the onset of muscle degeneration-regeneration, fluorescence confocal microscopy showed that there were no detectable differences in the pattern of Schwann cell distribution in the mdx compared to controls of the same age. Schwann cells had a diffuse pattern of distribution, covering the plaques of acetylcholine receptors. In adult mdx muscles, terminal Schwann cell processes filled the center of acetylcholine receptors islands, similar to nerve terminal distribution, at the majority of the junctions (n=200; 100%). Conversely, all of the adult control junctions (n=200) showed continuous processes of Schwann cells covering the continuous branches of acetylcholine receptors. These observations indicate that remodeling of the three components of the neuromuscular junction occurs only after the onset of the cycles of muscle fiber degeneration-regeneration, in the mdx mice.

Neuroma apendicular (obliteración fibrosa) asociado a microcarcinoide solitario / Neuroma of the appendix (fibrous obliteration) associated with solitary microcarcinoid

Informamos un caso de neuroma apendicular (obliteración fibrosa de la punta) asociado con microcarcinoide solitario del tercio medio del apéndice cecal. Esta lesión resulta de la proliferación neuromatosa con obliteración de la luz e hiperplasia de células endócrinas extraepiteliales. La inmunohitoquímica para proteína S-100, enolasa neurona específica (NSE) y factor de crecimiento epidérmico (EGF) resultaron positivos y la desmina, el antígeno epitelial de membrana (EMA) y la proteína fibrilar ácida glial (GFAP) fueron negativos. Lo anterior indica que la obliteración fibrosa del apéndice cecal es una proliferación de células de Schwann y no un proceso fibroblástico degenerativo. La hiperplasia de células endócrinas podría estimular por un lado, la proliferación de células de Schwann y por otro, inducir el crecimiento de carcinoides y así explicar esta interesante asociación

Ectomesenquimoma maligno; informe de un caso / Malignant ectomesen chimoma: report of a case

Se informan los hallazgos clínicos y patológicos de un ectomesenquimoma maligno de partes blandas. Los ectomesenquimomas malignos son tumores compuestos por derivados de la cresta neural y uno o más elementos mesenquimatosos malignos, por lo general rabdomiosarcoma, condrosarcoma, angiosarcoma y liposarcoma maligno y liposarcoma. En esta neoplasia, el tratamiento más adecuado es el quirúrgico, pues la quimioterapia y la radioterapia no parecen modifiar el curso de la enfermedad. En este caso el tratamiento fue quirúrgico, sin datos de actividad tumoral a los 16 meses subsecuentes a la operación.