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.

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.

Mesenchyme-mediated effects of retinoic acid during rat intestinal development

1997 ◽  
Vol 110 (10) ◽  
pp. 1227-1238 ◽  
Author(s):  
M. Plateroti ◽  
J.N. Freund ◽  
C. Leberquier ◽  
M. Kedinger
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cell ◽  
Polyclonal Antibodies ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Cell Polarization ◽  
Cell Interactions ◽  
Intestinal Cell ◽  
Cell Phenotype ◽  
Intestinal Development

In previous experiments we showed that intestinal development was dependent upon epithelial-mesenchymal cell interactions. The aim of this study was to investigate the possible role of retinoic acid (RA), a morphogenetic and differentiating agent, on the gut epithelial-mesenchymal unit. For this purpose we first analyzed the effects of a physiological dose of RA on 14-day fetal rat intestine using short-term organ culture experiments, or long-term grafts under the skin of nude mice. In these conditions, RA accelerated villus outgrowth and epithelial cell differentiation as assessed by the onset of lactase expression, and it also stimulated muscle and crypt formation. In order to analyze potential effects of RA mediated by mesenchymal cells, we isolated and characterized gut mucosa mesenchyme-derived cell cultures (mesenchyme-derived intestinal cell lines, MIC). These cells were shown to express mRNAs for retinoid binding proteins similar to those expressed in situ in the intestinal mesenchyme. MIC cells co-cultured with 14-day intestinal endoderms promoted endodermal cell adhesion and growth, and the addition of exogeneous RA enhanced epithelial cell polarization and differentiation assessed by cytokeratin and lactase immunostaining. Such a differentiating effect of RA was not observed on endodermal cells when cultured without a mesenchymal feeder layer or maintained in conditioned medium from RA-treated MIC cells. In the co-cultures, immunostaining of laminin and collagen IV with polyclonal antibodies, as well as alpha1 and beta1 laminin chains mRNAs (analyzed by RT-PCR) increased concurrently with the RA-enhanced differentiation of epithelial cells. It is worth noting that this stimulation by RA was also obvious on the mesenchymal cells cultured alone. These results show that RA plays a role in intestinal morphogenesis and differentiation. In addition, they indicate that RA acts on the mesenchymal cell phenotype and suggest that RA may modify the mesenchymal-epithelial cell interactions during intestinal development.

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.

Large Vulvar Lipoma in an Adolescent: A Case Report

JMS SKIMS ◽  
2011 ◽  
Vol 14 (1) ◽  
pp. 28-29
Author(s):  
R K Maurya ◽  
Pawan Kumar Singh ◽  
Sandeep Singh
Keyword(s):  
Case Report ◽  
Epithelial Cell ◽  
Adolescent Girl ◽  
Rare Case ◽  
Mesenchymal Cell ◽  
Benign Tumors ◽  
Melanocytic Tumors

Lipomas of vulva have been reported only rarely. Benign tumors of the vulva are normally classified according to their origin as epithelial cell tumors (e.g., keratinocytic, adnexal and ectopic tumors), or mesenchymal cell tumors (e.g., vascular, fibrous, muscular, neural, adipose and melanocytic tumors). Vulvar lipomas need to be differentiated from liposarcomas, which are rare but are very similar to lipomas clinically. Here we present a rare case of large vulvar lipoma in an adolescent girl. JMS 2011;14(1):28-29

Yolk transport in the ovarian follicle of the hen (Gallus domesticus): lipoprotein-like particles at the periphery of the oocyte in the rapid growth phase

1979 ◽  
Vol 39 (1) ◽  
pp. 257-272 ◽  
Author(s):  
M.M. Perry ◽  
A.B. Gilbert
Keyword(s):  
Basal Lamina ◽  
Granulosa Cells ◽  
Plasma Membranes ◽  
Ovarian Follicle ◽  
Cell Loss ◽  
Coated Vesicles ◽  
Morphological Alteration ◽  
Tissue Preparation ◽  
Very Low Density Lipoproteins ◽  
Thin Sections

Thin sections of the oocyte periphery and surrounding granulosa layer from 1–5 day preovulatory follicles were examined by transmission electron microscopy. With the use of certain procedures in tissue preparation, notably the tannic acid method, numerous particles in the range of 15–40 nm with a mean diameter of 27 nm were observed in both extra- and intracellularly. The particles were abundant in the granulosa basal lamina, in the spaces between the granulosa cells and in the perivitelline space. They appeared to adhere to the oolemma as a continuous double layer which was also observed to line the coated vesicles, 200–350 nm in diameter, invaginating from the oolemma. The layer of particles was not found on the plasma membranes of the granulosa cells, nor were particles present within the cells. In the peripheral cytoplasm of the oocyte the yolk spheres, ranging upwards from 250 nm diameter, were membrane-bound and contained tightly packed particles similar to those on the oolemma. Bodies displaying features intermediate between coated vesicles and yolk spheres suggested that, on entry into the cell, loss of the cytoplasmic coat and obliteration of the vesicular lumen gave rise to nascent yolk spheres which then fused together to form the larger spheres. The extracellular layer, coated vesicles and smaller yolk spheres were absent in oocytes fixed after a 10-min delay. The evidence indicated that 27-nm particles were transferred from the basal lamina to the oocyte surface via the intergranulosa cell channels, incorporated into the cell by adsorptive endocytosis and then transferred to the yolk spheres with little morphological alteration. The identity of the particles with very low density lipoproteins, the major components of the yolk solids, was discussed.

Tissue distribution and vitamin D dependence of IMCAL in the rat

1987 ◽  
Vol 253 (3) ◽  
pp. G411-G419
Author(s):  
S. Kowarski ◽  
L. A. Cowen ◽  
M. T. Takahashi ◽  
D. Schachter
Keyword(s):  
Vitamin D ◽  
Tissue Distribution ◽  
Intestinal Mucosa ◽  
Plasma Membranes ◽  
Duodenal Mucosa ◽  
Calcium Flux ◽  
Small Intestinal Mucosa ◽  
Calcium Diet ◽  
High Calcium ◽  
Cecal Mucosa

Integral membrane calcium-binding protein (IMCAL) is a vitamin D-dependent integral membrane protein that binds calcium with relatively high affinity (J. Biol. Chem. 225: 10834-10840, 1980). Specific immunoassays for IMCAL utilizing rabbit polyclonal and mouse monoclonal antibodies were developed and applied to studies of its tissue distribution and regulation by vitamin D3 and dietary calcium in the rat. The results indicate that vitamin D-dependent, cross-reactive protein is present in small intestinal mucosa, cecal mucosa, bone, kidney, brain, testis, heart, lung, spleen, and skin. Rats maintained on a low- (0.02%) compared with & high- (2.0%) calcium diet had significantly higher content of IMCAL in duodenal mucosa, cecal mucosa, bone, kidney, brain, testis, and heart. Treatment of rats on the high-calcium diet with 1,25-dihydroxyvitamin D3 increased the IMCAL content of the duodenal mucosa, cecal mucosa, and kidney. The widespread tissue distribution of vitamin D-dependent IMCAL, its close correlation in intestinal mucosa with the calcium transport mechanism, and its occurrence in isolated preparations of enterocyte plasma membranes (microvillus and basolateral membranes) suggest that the protein is involved in the regulation of calcium flux in a number of cell types.

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 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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