Acetylcholinesterase (AChE) and pseudocholinesterase (BuChE) activity distribution pattern in early developing chick limbs

Development ◽  
1985 ◽  
Vol 86 (1) ◽  
pp. 89-108
Author(s):  
Carla Falugi ◽  
Margherita Raineri
Keyword(s):  
Plasma Membrane ◽  
Basal Lamina ◽  
Ache Activity ◽  
Quantitative Methods ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Regional Localization ◽  
Stage Of Development ◽  
Limb Morphogenesis ◽  
Cell Processes

The distribution of acetylcholinesterase (AChE) and pseudocholinesterase (BuChE) activities was studied by histochemical, quantitative and electrophoretical methods during the early development of chick limbs, from stage 16 to stage 32 H.H. (Hamburger & Hamilton, 1951). By quantitative methods, true AChE activity was found, and increased about threefold during the developmental period, together with a smaller amount of BuChE which increased more rapidly in comparison with the AChE activity from stage 25 to 32 H.H. Cholinesterase activity was histochemically localized mainly in interacting tissues, such as the ectoderm (including the apical ectodermal ridge) and the underlying mesenchyme. True AChE was histochemically localized around the nuclei and on the plasma membrane of ectodermal (including AER) and mesenchymal cells, and at the plasma membrane of mesenchymal cell processes reaching the basal lamina between the ectoderm and the mesenchyme. AChE together with BuChE activity was found in the basal lamina between the ectoderm and the mesenchyme, in underlying mesenchymal cells and in deeper mesenchymal cells, especially during their transformation into unexpressed chondrocytes. During limb morphogenesis, the cellular and regional localization of the enzyme activities showed variations depending on the stage of development and on the occurrence of interactions. The possibility of morphogenetic functions of the enzyme is discussed.

scholarly journals STRUCTURAL FEATURES OF THE EPITHELIO-MESENCHYMAL INTERFACE OF RAT DUODENAL MUCOSA DURING DEVELOPMENT

1972 ◽  
Vol 52 (3) ◽  
pp. 577-588 ◽  
Author(s):  
Minnie Mathan ◽  
John A. Hermos ◽  
Jerry S. Trier
Keyword(s):  
Epithelial Cell ◽  
Lamina Propria ◽  
Basal Lamina ◽  
Plasma Membranes ◽  
Mesenchymal Cell ◽  
Duodenal Mucosa ◽  
Mesenchymal Cells ◽  
Adult Rats ◽  
Contact Sites ◽  
Cell Processes

In fetal rats 5–7 days before birth, the duodenal epithelium is separated from mesenchymal cells by a well-defined basal lamina. By 3–4 days before birth, when small rudimentary villi are first seen, direct contact between epithelial and mesenchymal cells occurs by means of epithelial cell cytoplasmic processes which project through gaps in the basal lamina into the lamina propria. At contact sites, the epithelial and mesenchymal cell plasma membranes were less than 100 A apart but membrane fusion was not seen. In number and size these epithelial cell processes increase strikingly during the last 2 days of gestation, and they persist in large numbers until 7–10 days after birth. Thereafter, they decrease gradually in both number and size until 3–4 wk after birth, when the morphology of the epithelio-mesenchymal interface resembles that seen in adult rats, i.e., there are only rare epithelial cell processes which penetrate deeply into the lamina propria. The presence of a large number of epithelio-mesenchymal contact sites during the period of rapid growth and differentiation of duodenal mucosa may reflect epithelio-mesenchymal cell interactions which may facilitate the maturation of the duodenal mucosa.

scholarly journals Basal lamina directs acetylcholinesterase accumulation at synaptic sites in regenerating muscle.

1985 ◽  
Vol 101 (3) ◽  
pp. 735-743 ◽  
Author(s):  
L Anglister ◽  
U J McMahan
Keyword(s):  
Plasma Membrane ◽  
Neuromuscular Junction ◽  
Basal Lamina ◽  
Acetylcholine Receptors ◽  
Skeletal Muscles ◽  
Ache Activity ◽  
Neuromuscular Junctions ◽  
Muscle Fibers ◽  
Synaptic Cleft

In skeletal muscles that have been damaged in ways which spare the basal lamina sheaths of the muscle fibers, new myofibers develop within the sheaths and neuromuscular junctions form at the original synaptic sites on them. At the regenerated neuromuscular junctions, as at the original ones, the muscle fibers are characterized by junctional folds and accumulations of acetylcholine receptors and acetylcholinesterase (AChE). The formation of junctional folds and the accumulation of acetylcholine receptors is known to be directed by components of the synaptic portion of the myofiber basal lamina. The aim of this study was to determine whether or not the synaptic basal lamina contains molecules that direct the accumulation of AChE. We crushed frog muscles in a way that caused disintegration and phagocytosis of all cells at the neuromuscular junction, and at the same time, we irreversibly blocked AChE activity. New muscle fibers were allowed to regenerate within the basal lamina sheaths of the original muscle fibers but reinnervation of the muscles was deliberately prevented. We then stained for AChE activity and searched the surface of the new muscle fibers for deposits of enzyme they had produced. Despite the absence of innervation, AChE preferentially accumulated at points where the plasma membrane of the new muscle fibers was apposed to the regions of the basal lamina that had occupied the synaptic cleft at the neuromuscular junctions. We therefore conclude that molecules stably attached to the synaptic portion of myofiber basal lamina direct the accumulation of AChE at the original synaptic sites in regenerating muscle. Additional studies revealed that the AChE was solubilized by collagenase and that it remained adherent to basal lamina sheaths after degeneration of the new myofibers, indicating that it had become incorporated into the basal lamina, as at normal neuromuscular junctions.

Ultrastructural identification of extracellular matrix and cell surface components during limb morphogenesis in man

Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 1-18
Author(s):  
Robert O. Kelley
Keyword(s):  
Extracellular Matrix ◽  
Cell Surface ◽  
Basal Lamina ◽  
Mesenchymal Cell ◽  
Ruthenium Red ◽  
Human Hand ◽  
Binding Characteristics ◽  
Limb Morphogenesis ◽  
Testicular Hyaluronidase

Development of the human hand plate (stages 16–17) has been analyzed with emphasis on differentiation of elements within the extracellular matrix and the composition of the mesenchymal cell surface. The epithelial—mesenchymal interface contains a basal lamina and a sublaminar matrix exhibiting: (a) collagen fibrils with characteristic 63–64 nm banding; (b) non-banded filaments, 10–15 nm in diameter; (c) ruthenium red-positive particles, 12–15 nm in diameter; and (d) attenuated threads, 3·5–5·0 nm in diameter which interconnect particles, fibrils, filaments and the basal lamina. Processes of mesenchymal cells penetrate this matrix network. In addition to staining with ruthenium red, components of basal laminae bind to ferritin-conjugated Concanavalin A, greatest binding being localized on the mesenchymal surface of the lamina. Asymmetry of binding is removed by incubation of exposed laminae with trypsin (5 µg/ml). Regional differences in these staining and binding characteristics within the subepithelial matrix have not been observed in the hand plate. However, precartilaginous extracellular zones deep within the plate are notably unstructured in comparison to the sublaminar region. Ruthenium red-positive materials at mesenchymal cell surfaces display sensitivity to testicular hyaluronidase, Pronase and trypsin but resist removal with neuraminidase and EDTA. These features of the substrate in situ may be important in the regulation of mesenchymal cell behavior during limb morphogenesis in man.

The fine structure of Leucocytozoon simondi. V. The oocyst

1972 ◽  
Vol 50 (6) ◽  
pp. 707-711 ◽  
Author(s):  
Sherwin S. Desser
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Fine Structure ◽  
Basal Lamina ◽  
Central Core ◽  
Granular Endoplasmic Reticulum ◽  
Midgut Epithelium ◽  
Stage Of Development ◽  
Peripheral Cytoplasm

Following penetration through the midgut epithelium of Simulium rugglesi, ookinetes of Leucocytezoon simondi round up beneath the basal lamina and transform into young oocysts. These spherical, walled structures contain a large central core of crystalloid material. Dividing nuclei are seen in the peripheral cytoplasm, which is characterized by several concentric layers of granular endoplasmic reticulum. In a succeeding stage of development the trilaminar plasma membrane appears intermittently doubled, and bud-like outgrowths occur in these thickened areas. At this stage the crystalloid material is dispersed throughout the cytoplasm. A nucleus, an elongate mitochondrion, and some crystalloid material move into each forming sporozoite, which continues to grow at the expense of the residual cytoplasm.

An ultrastructural and morphometric analysis of an in vivo contact guidance system

Development ◽  
1987 ◽  
Vol 101 (2) ◽  
pp. 363-381
Author(s):  
A. Wood ◽  
P. Thorogood
Keyword(s):  
Cell Migration ◽  
Morphometric Analysis ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Contact Guidance ◽  
Cell Phenotype ◽  
Cell Processes ◽  
Computer Based ◽  
The Mean

The pectoral fin bud of the developing teleost embryo contains a highly ordered extracellular matrix of collagenous fibrils, called ‘actinotrichia’. During invasion of the fin fold, mesenchymal cells, migrating distally from the base of the fin, become contact aligned by the actinotrichial fibrils. Behavioural aspects of this response have previously been studied using Nomarski differential interference contrast microscopy and time-lapse video recording (Wood & Thorogood, 1984). Here we present an ultrastructural description of these cells and their matrix associations and a computer- based morphometric analysis of selected parameters within the migration substratum, relevant to this in vivo ‘contact guidance’ phenomenon. The study shows that a differentiated and aligned matrix of actinotrichial fibrils can be detected before invasion of the fin fold, at levels up to 40μm distal to the advancing mesenchymal cell margin. Subsequently, during invasion of the fin fold, aligned mesenchymal cells and processes are almost exclusively associated with actinotrichia and not the intervening surface of the epithelial basal lamina. However, aligned cell processes appear to avoid the smaller actinotrichia and at late stages of development 87á0% of actinotrichia without cell process contacts are distributed at the lower end of the size range. Study of cell ultrastructure revealed a complete absence of cytoskeletal organization within this mesenchymal cell population, although cytoskeletal components are clearly visible in adjacent epithelia. The computer-based morphometric survey of the migration substratum has shown a gradual but progressive increase in the mean diameter of actinotrichia at a level at which distal cell processes are first detectable in sections of fins. However, at similar levels over the same period the mean value for interactinotrichial spacings remained virtually constant. These results suggest that the spacing between actinotrichia is not significant in contributing to progressive changes in mesenchymal cell phenotype, but that the actinotrichia themselves are strongly implicated in providing the guidance cues to direct cell migration within the developing fin and the initiation of cell migration. These findings are discussed in the general context of cell movement and contact guidance both in vivo and in vitro.

Cellular Invasion and Matrix Degradation, a Different Type of Matrix-Degrading Cells in the Cartilage of Catfish (Clarias gariepinus) and Japanese Quail Embryos (Coturnix coturnix japonica)

2019 ◽  
Vol 25 (05) ◽  
pp. 1283-1292 ◽  
Author(s):  
Soha A. Soliman ◽  
Basma Mohamed Kamal ◽  
Hanan H. Abd-Elhafeez
Keyword(s):  
Clarias Gariepinus ◽  
Mesenchymal Cell ◽  
Cell Types ◽  
Cartilage Degradation ◽  
Mesenchymal Cells ◽  
Cartilage Growth ◽  
Cellular Invasion ◽  
Transmission Electron ◽  
Cell Processes ◽  
Different Cell Types

AbstractWe previously studied the phenomena of the mesenchymal cell-dependent mode of cartilage growth in quail and catfish. Thus, we selected the two cartilage models in which mesenchymal cells participate in their growth. In such models, cartilage degradation occurred to facilitate cellular invasion. The studies do not explain the nature of the cartilage degrading cells. The current study aims to explore the nature of the cartilage-degrading cells using transmission electron microscopy (TEM) and immunohistochemistry. Samples of cartilage have been isolated from the air-breathing organ of catfish and the cartilage of the prospective occipital bone of quail embryos. Samples have been processed for TEM and immunohistochemistry. We found that two different cell types are involved in cartilage degradation; the macrophage in the cartilage of catfish and mesenchymal cells in the cartilage of the quail. Areas of cellular invasion in both catfish cartilage and quail embryo cartilage had an immunological affinity for MMP-9. In catfish, cartilage-degrading cells had identical morphological features of macrophages, whereas in quail embryos, cartilage-degrading cells were mesenchymal-like cells which had cell processes rich in vesicles and expressed CD117. Further study should consider the role of macrophage and mesenchymal cells during cartilage degradation. This could be valuable to be applied to remove the defective cartilage matrix formed in osteoarthritic patients to improve cartilage repair strategies.

Fibrogenesis IV. Fibrosis and inflammatory bowel disease: cellular mediators and animal models

2000 ◽  
Vol 279 (4) ◽  
pp. G653-G659 ◽  
Author(s):  
Jolanta B. Pucilowska ◽  
Kristen L. Williams ◽  
P. Kay Lund
Keyword(s):  
Sulfonic Acid ◽  
Genetic Manipulation ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Acute Injury ◽  
Ethanol Administration ◽  
Cell Phenotype ◽  
Trinitrobenzene Sulfonic Acid ◽  
Intestinal Fibrosis ◽  
Cellular Mediators

The cellular mediators of intestinal fibrosis and the relationship between fibrosis and normal repair are not understood. Identification of the types of intestinal mesenchymal cells that produce collagen during normal healing and fibrosis is vital for elucidating the answers to these questions. Acute injury may cause normal mesenchymal cells to convert to a fibrogenic phenotype that is not maintained during normal healing but may lead to fibrosis when inappropriately sustained. Proliferation of normal or fibrogenic mesenchymal cells may lead to muscularis overgrowth associated with fibrosis. The presence of increased numbers of vimentin-positive cells within fibrotic, hypertrophied muscularis in Crohn's disease suggests that changes in mesenchymal cell phenotype and number may indeed be associated with fibrosis. Fibrosis is induced in rats by peptidoglycan polysaccharides or trinitrobenzene sulfonic acid-ethanol administration, but inducing fibrosis in mice has been technically challenging. The development of current mouse models of colitis, such as dextran sodium sulfate or trinitrobenzene sulfonic acid-ethanol administration, into models of fibrosis will allow us to use genetic manipulation to study molecular mediators of fibrosis.

scholarly journals Acetylcholinesterase from the motor nerve terminal accumulates on the synaptic basal lamina of the myofiber.

1991 ◽  
Vol 115 (3) ◽  
pp. 755-764 ◽  
Author(s):  
L Anglister
Keyword(s):  
Basal Lamina ◽  
Ache Activity ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Synaptic Cleft ◽  
Motor Nerve Terminal ◽  
Nerve Terminals ◽  
Axon Terminals ◽  
Muscle Nerve ◽  
Almost All

Acetylcholinesterase (AChE) in skeletal muscle is concentrated at neuromuscular junctions, where it is found in the synaptic cleft between muscle and nerve, associated with the synaptic portion of the myofiber basal lamina. This raises the question of whether the synaptic enzyme is produced by muscle, nerve, or both. Studies on denervated and regenerating muscles have shown that myofibers can produce synaptic AChE, and that the motor nerve may play an indirect role, inducing myofibers to produce synaptic AChE. The aim of this study was to determine whether some of the AChE which is known to be made and transported by the motor nerve contributes directly to AChE in the synaptic cleft. Frog muscles were surgically damaged in a way that caused degeneration and permanent removal of all myofibers from their basal lamina sheaths. Concomitantly, AChE activity was irreversibly blocked. Motor axons remained intact, and their terminals persisted at almost all the synaptic sites on the basal lamina in the absence of myofibers. 1 mo after the operation, the innervated sheaths were stained for AChE activity. Despite the absence of myofibers, new AChE appeared in an arborized pattern, characteristic of neuromuscular junctions, and its reaction product was concentrated adjacent to the nerve terminals, obscuring synaptic basal lamina. AChE activity did not appear in the absence of nerve terminals. We concluded therefore, that the newly formed AChE at the synaptic sites had been produced by the persisting axon terminals, indicating that the motor nerve is capable of producing some of the synaptic AChE at neuromuscular junctions. The newly formed AChE remained adherent to basal lamina sheaths after degeneration of the terminals, and was solubilized by collagenase, indicating that the AChE provided by nerve had become incorporated into the basal lamina as at normal neuromuscular junctions.

scholarly journals The endosome is a master regulator of plasma membrane collagen fibril assembly

2021 ◽  
Author(s):  
Joan Chang ◽  
Adam Pickard ◽  
Richa Garva ◽  
Yinhui Lu ◽  
Donald Gullberg ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Circadian Clock ◽  
Collagen Fibril ◽  
Collagen Fibrils ◽  
Protein Mass ◽  
Stage Of Development ◽  
Collagen Secretion ◽  
Total Protein Mass ◽  
Vacuolar Protein ◽  
Membrane Collagen

abstractCollagen fibrils are the principal supporting elements in vertebrate tissues. They account for 25% of total protein mass, exhibit a broad range of size and organisation depending on tissue and stage of development, and can be under circadian clock control. Here we show that the remarkable dynamic pleomorphism of collagen fibrils is underpinned by a mechanism that distinguishes between collagen secretion and initiation of fibril assembly, at the plasma membrane. Collagen fibrillogenesis occurring at the plasma membrane requires vacuolar protein sorting (VPS) 33b (which is under circadian clock control), collagen-binding integrin-α11 subunit, and is reduced when endocytosis is inhibited. Fibroblasts lacking VPS33b secrete soluble collagen without assembling fibrils, whereas constitutive over-expression of VPS33b increases fibril number with loss of fibril rhythmicity. In conclusion, our study has identified the mechanism that switches secretion of collagen (without forming new fibrils) to new collagen fibril assembly, at the plasma membrane.

scholarly journals Cell Elongation Induces Laminin α2 Chain Expression in Mouse Embryonic Mesenchymal Cells

1999 ◽  
Vol 147 (6) ◽  
pp. 1341-1350 ◽  
Author(s):  
Nand K. Relan ◽  
Yan Yang ◽  
Safedin Beqaj ◽  
Jeffrey H. Miner ◽  
Lucia Schuger
Keyword(s):  
Cell Shape ◽  
Contractile Activity ◽  
Congenital Muscular Dystrophy ◽  
Mesenchymal Cell ◽  
Specific Protein ◽  
Mesenchymal Cells ◽  
Bronchial Smooth Muscle ◽  
Functional Studies ◽  
Low Levels ◽  
Dy Mouse

Bronchial smooth muscle (SM) mesenchymal cell precursors change their shape from round to spread/elongated while undergoing differentiation. Here we show that this change in cell shape induces the expression of laminin (LM) α2 chain not present in round mesenchymal cells. LM α2 expression is reversible and switched on and off by altering the cell's shape in culture. In comparison, the expression of LM β1 and γ1 remains unchanged. Functional studies showed that mesenchymal cell spreading and further differentiation into SM are inhibited by an antibody against LM α2. Dy/dy mice express very low levels of LM α2 and exhibit congenital muscular dystrophy. Lung SM cells isolated from adult dy/dy mice spread defectively and synthesized less SM α-actin, desmin, and SM-myosin than controls. These deficiencies were completely corrected by exogenous LM-2. On histological examination, dy/dy mouse airways and gastrointestinal tract had shorter SM cells, and lungs from dy/dy mice contained less SM-specific protein. The intestine, however, showed compensatory hyperplasia, perhaps related to its higher contractile activity. This study therefore demonstrated a novel role for the LM α2 chain in SM myogenesis and showed that its decrease in dy/dy mice results in abnormal SM.

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