RESUMO
The myotendinous junction (MTJ) is an interface that different stimuli alter their morphology. One of the main stimuli to promote alterations in the MTJ morphology is physical exercise. The present study aimed to investigate the morphology and molecular MTJ adaptations of biceps brachii muscle in adult Wistar rats submitted to different ladder-based protocols. Forty Wistar rats (90 days old) were divided into four groups: Sedentary (S), Climbing (C), Overload Climbing (OC), Climbing, and Overload Climbing (COC). The results of light microscopy demonstrated the cell and collagen tissue reorganization in the experimental groups. The sarcomeres lengths of different regions showed a particular development according to the specific protocols. The sarcoplasmic invaginations and evaginations demonstrated positive increases that promoted the myotendinous interface development. In the extracellular matrix, the structures presented an increase principally in the COC group. Finally, the immunofluorescence analysis showed the telocytes disposition adjacent to the MTJ region in all experimental groups, revealing their network organization. Thus, we concluded that the different protocols contributed to the morphological adaptations with beneficial effects in distinct ways of tissue and cellular development and can be used as a model for MTJ remodeling to future proteomic and genetic analysis.
RESUMO
Neuroblastoma (NB) is the most common pediatric extracranial solid tumor. It arises during development of the sympathetic nervous system. Netrin-4 (NTN4), a laminin-related protein, has been proposed as a key factor to target NB metastasis, although there is controversy about its function. Here, we show that NTN4 is broadly expressed in tumor, stroma and blood vessels of NB patient samples. Furthermore, NTN4 was shown to act as a cell adhesion molecule required for the migration induced by Neogenin-1 (NEO1) in SK-N-SH neuroblastoma cells. Therefore, we propose that NTN4, by forming a ternary complex with Laminin γ1 (LMγ1) and NEO1, acts as an essential extracellular matrix component, which induces the migration of SK-N-SH cells.
Assuntos
Movimento Celular , Regulação Neoplásica da Expressão Gênica , Laminina/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Netrinas/metabolismo , Neuroblastoma/patologia , Receptores de Superfície Celular/metabolismo , Adesão Celular , Feminino , Humanos , Lactente , Masculino , Neuroblastoma/metabolismo , Células Tumorais CultivadasRESUMO
Glándulas salivales de pacientes con síndrome de Sjõgren presentan un aumento en la degradación de componentes de la lámina basal (LB, laminina y colágeno IV) y estroma (colágenos I y III y fibronectina). Estos cambios se correlacionan con un desbalance en la expresión y actividad de metaloproteinasas y sus inhibidores titulares (MMP/TIMP) que desorganiza la LB de acinos y ductos. Esta desorganización es concomitante a una sobreexpresión de lamininas -1 y -5 y a la degradación de nidógenos 1 y -2, que tienen como función establecer puentes de conexión entre laminina y colágeno IV. Cambios post-transcripcionales de la integrina alfa 6 beta 4 están correlacionados con una drástica redistribución de beta 4 en acinos con LB desorganizadas. Estos resultados sugieren que alteraciones en la adhesión célula-matriz y en la formación de contactos célula-célula pueden modificar la señalización de la integrina alfa 6 beta 4 induciendo muerte celular cuando hay una severa interrupción de la célula acinar con la LB.
Increased degradation of basal lamina (BL, laminin and type IV collagen) and stroma (type I and III collagens, and fibronectin) proteins have been observed in salivary glands of patients with Sjõgrens syndrome. Such changes are associated with imbalanced expression and activity of extracellular matrix metalloproteinases and their tissue inhibitors (MMPs/TIMPs), which contribute to disorganization of the parenchyma basal lamina. Disorganization of the basal lamina is paralleled by an overexpression of laminin-1and -5 and the degradation of nidogens 1 and -2: linker proteins that help maintain the integrity of type IV collagen and laminin networks.Additionally, post-transcriptional changes in alpha 6 beta 4 integrin are associated with a dramatic redistribution of beta 4 in acini, particularly where perturbations in BL organization were apparent. These findings are taken to suggest that changes in acinar cell-matrix adhesion and cell-cell contact formation may alter alpha 6beta 4 integrin signaling, triggering cell death only when severe disruption of cell-BL attachment occurs.
Assuntos
Humanos , Matriz Extracelular , Glândulas Salivares/patologia , Laminina/fisiologia , Membrana Basal/patologia , Síndrome de Sjogren/patologia , Glândulas Salivares/imunologia , Metaloproteinases da Matriz , Membrana Basal/imunologia , Síndrome de Sjogren/imunologia , Síndrome de Sjogren/metabolismoRESUMO
In the present study human synovial bursa specimens were examined by light and transmission electron microscopy. For light microscopical investigation the bursa tissue was stained with azan, haematoxylin-eosin and monoclonal antibodies (CD14, CD33, CD36, CD68, laminin). For electron microscopical investigation the bursa specimens were fixated with Karnovsky's solution and 1,5% osmium tetroxide (Os0(4)) in water distilled and contrasted with 5% uranylacetate and embedded in Epon®. For the first time the antigenic phenotype was characterized and conclusions were drawn about the origin of the synovial bursa cells. Histologically the bursa was divided in two distinct layers; the intima, which is formed by a lining layer and a lamina propria, and a subintimal layer. The intima consisted of macrophage like (type I) and fibroblast like cells (type II). According to the immunohistochemical staining and the electron microscopy the type I cell seemed to be a bone marrow derived monocyte and the more frequently seen type II cell was derived from subintimal fibroblasts. The intimal bursa cell frequently interdigitated and usually communicated by their filopodia (indirect cell-cell-communication). Neither tight or gap junctions nor desmosomes could be documented. Although there was no evidence for the existence of a basal lamina, a concentration of extracellular matrix components beyond the bursa cells was observed. In our study there was no accumulation of laminin around the bursal cells, but striking was a vascular bundle of the intima subintima border zone, which was positive for laminin and CD68 and separated the intima from the subintima. In our opinion this histological structure plays an important role in the regeneration of the lining cells and acts like a barrier between bursa and blood.
En el presente estudio se examinaron bolsas sinoviales humanas a través de microscopía de luz y electrónica de transmisión. Para la microscopía de luz, el tejido de las bolsas se tiñó con Azan, H-E y anticuerpos monoclonales (CD14, CD33, CD36, CD68, laminina). Para la microscopía electrónica las bolsas fueron fijadas con solución de Karnovsky y tetróxido de osmio al 1,5% (Os04) en agua destilada y contrastada con acetato de uranilo al 5% y embebido en Epon®. En primera instada, el fenotipo antigénico fue caracterizado, concluyéndose acerca del origen de las células que componen la bolsa sinovial. Histológicamente la bolsa fue dividida en dos capas distintas - la íntima - la cual es formada por una capa lineal y una lámina propia, y, una subintima. La íntima consistió en células parecidas a macrófagos (Tipo I) y células semejantes a fibroblastos (Tipo II). De acuerdo a la tinción inmunohistoquímica y a la microscopía electrónica, las células tipo I parecen provenir de la médula ósea derivada de monocitos y el más frecuente tipo celular II fue derivadado de los fibroblastos de la subintima. Frecuentemente las células de la íntima de la bolsa se interdigitaban y usualmente se comunicaban a través de sus prolongaciones (comunicación célula indirecta-célula). No se observaron ni uniones abiertas, ni cerradas, ni desmosomas. Aunque no hubo evidencia de la existencia de una lámina basal, se observó una concentración de componentes de matriz extracelular más allá de las células de la bolsa. No hubo acumulación de laminina alrededor de estas células, pero destacada era una banda vascular de la zona límite entre íntima y subintima, la cual fue positiva para laminina y CD68 la cual separaba la íntima de la subintima. En nuestra opinión esta estructura histológica juega un importante rol en la regeneración de las células lineales y actúa como una barrera entre la bolsa y la sangre.