In vitro Interactions of Endometrial Stromal and Epithelial Cells in Matrigel: Reorganization of the Extracellular Matrix

Pathobiology ◽  
1994 ◽  
Vol 62 (2) ◽  
pp. 104-108 ◽  
Author(s):  
Helmut Hopfer ◽  
Clifford A. Rinehart Jr ◽  
Günter Vollmer ◽  
David G. Kaufman
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
In Vitro Interactions

Developmental aspects of secondary palate formation

Development ◽  
1976 ◽  
Vol 36 (2) ◽  
pp. 225-245
Author(s):  
Robert M. Greene ◽  
Robert M. Pratt
Keyword(s):  
Extracellular Matrix ◽  
Cell Death ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Hydrolytic Enzymes ◽  
Cellular Adhesion ◽  
Control Mechanisms ◽  
Adhesive Interaction ◽  
Secondary Palate

Research on development of the secondary palate has, in the past, dealt primarily with morphological aspects of shelf elevation and fusion. The many factors thought to be involved in palatal elevation, such as fetal neuromuscular activity and growth of the cranial base and mandible, as well as production of extracellular matrix and contractile elements in the palate, are mostly based on gross, light microscopic, morphometric or histochemical observations. Recently, more biochemical procedures have been utilized to describe palatal shelf elevation. Although these studies strongly suggest that palatal extracellular matrix plays a major role in shelf movement, interpretation of these data remains difficult owing to the complexity of tissue interactions involved in craniofacial development. Shelf elevation does not appear to involve a single motive factor, but rather a coordinated interaction of all of the abovementioned developmental events. Further analysis of mechanisms of shelf elevation requires development of new, and refinement of existing, in vitro procedures. A system that enables one to examine shelf elevation in vitro would allow more meaningful analysis of the relative importance of the various components in shelf movement. Much more is known about fusion of the palatal shelves, owing in large part to in vitro studies. Fusion of the apposing shelves, both in vivo and in vitro, is dependent upon adhesion and cell death of the midline epithelial cells. Adhesion between apposing epithelial surfaces appears to involve epithelial cell surface macromolecules. Further analysis of palatal epithelial adhesion should be directed towards characterization of those cell surface components responsible for this adhesive interaction. Midline epithelial cells cease DNA synthesis 24–36 h before shelf elevation and contact, become active in the synthesis of cell surface glycoproteins, and subsequently manifest morphological signs of necrosis. Death of the midline epithelial cells is thought to involve a programmed, lysosomal-mediated autolysis. Information regarding the appearance, distribution and quantitation of epithelial hydrolytic enzymes is needed. The control mechanisms which regulate adhesiveness and cell death in the palatal epithelium are not fully understood. Although palatal epithelial-mesenchymal recombination experiments have demonstrated a close relationship between the underlying mesenchyme and the differentiating epithelium, the molecular mechanism of interaction remains unclear. Recently cyclic nucleotides have been implicated as possible mediators of palatal epithelial differentiation. The developing secondary palate therefore offers a system whereby one can probe a variety of developmental phenomena. Cellular adhesion, programmed cell death and epithelial- mesenchymal interactions are all amenable to both morphological as well as bio- chemical analysis. Although research in the field of secondary palate development has been extensive, there still remain many provocative questions relating to normal development of this structure.

In vitro interactions between epithelial cells and Gyrodactylus derjavini

2000 ◽  
Vol 74 (3) ◽  
pp. 203-208 ◽  
Author(s):  
K. Buchmann ◽  
C.V. Nielsen ◽  
J. Bresciani
Keyword(s):  
Tissue Culture ◽  
Epithelial Cells ◽  
Cell Cultures ◽  
Culture Medium ◽  
Epithelioma Papulosum Cyprini ◽  
Skin Responses ◽  
Enzyme Reactivity ◽  
In Vitro Interactions

AbstractSkin responses of fish to various parasites have been shown to involve various immunologically competent cells producing factors which guide the reactions of epithelial cells. However, the present study has demonstrated that a monoculture of epithelial cells has the ability to encapsulate and partially degrade ectoparasites without involvement of leukocytes. The ectoparasitic monogeneanGyrodactylus derjavini was kept on a monolayer of Epithelioma Papulosum Cyprini (EPC) cells in 24-well multidishes supplied with tissue culture medium. Gyrodactylus derjavini did not reproduce but survived an incubation period of up to139 h in the system. Due to sterile conditions, dead gyrodactylids were not subjected to microbial degradation and remained intact for several weeks. However, at 40 days G. derjavini was overgrown by EPC-cells and became partly degraded during the following 15 days. Analysis of enzyme reactivity in EPC-cells showed reactions for ten enzymes including esterases, amidases, phosphatases and phosphohydrolases. No marked differences for the ten enzymes between cell cultures with and without the ectoparasites were found but it cannot be excluded that some of these enzymes took part in parasite degradation. The study showed the in vitro capability of epithelial cells to interact, encapsulate and degrade G. derjavini without the involvement of leukocytes. This response probably is non-specific and will not exclude that various immunocompetent cells and their products normally optimize and accelerate elimination of invading parasites in vivo.

Dynamic extracellular matrix stiffening induces a phenotypic transformation and a migratory shift in epithelial cells

2020 ◽  
Vol 12 (6) ◽  
pp. 161-174
Author(s):  
Shane C Allen ◽  
Jessica A Widman ◽  
Anisha Datta ◽  
Laura J Suggs
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Soft Tissue Tumors ◽  
Tumor Formation ◽  
Matrix Stiffness ◽  
Mesenchymal Transition ◽  
Cell Clusters

Abstract Soft tissue tumors, including breast cancer, become stiffer throughout disease progression. This increase in stiffness has been shown to correlate to malignant phenotype and epithelial-to-mesenchymal transition (EMT) in vitro. Unlike current models, utilizing static increases in matrix stiffness, our group has previously created a system that allows for dynamic stiffening of an alginate–matrigel composite hydrogel to mirror the native dynamic process. Here, we utilize this system to evaluate the role of matrix stiffness on EMT and metastasis both in vitro and in vivo. Epithelial cells were seen to lose normal morphology and become protrusive and migratory after stiffening. This shift corresponded to a loss of epithelial markers and gain of mesenchymal markers in both the cell clusters and migrated cells. Furthermore, stiffening in a murine model reduced tumor burden and increased migratory behavior prior to tumor formation. Inhibition of FAK and PI3K in vitro abrogated the morphologic and migratory transformation of epithelial cell clusters. This work demonstrates the key role extracellular matrix stiffening has in tumor progression through integrin signaling and, in particular, its ability to drive EMT-related changes and metastasis.

scholarly journals Cells that emerge from embryonic explants produce fibers of type IV collagen.

1985 ◽  
Vol 101 (4) ◽  
pp. 1175-1181 ◽  
Author(s):  
J M Chen ◽  
C D Little
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Basement Membrane ◽  
Type Iv Collagen ◽  
Polyclonal Antibodies ◽  
Mouse Lung ◽  
Embryonic Mouse ◽  
Type Iv ◽  
Collagen Substratum

Double immunofluorescence staining experiments designed to examine the synthesis and deposition of collagen types I and IV in cultured explants of embryonic mouse lung revealed the presence of connective tissue-like fibers that were immunoreactive with anti-type IV collagen antibodies. This observation is contrary to the widely accepted belief that type IV collagen is found only in sheet-like arrangements beneath epithelia or as a sheath-like layer enveloping bundles of nerve or muscle cells. The extracellular matrix produced by cells that migrate from embryonic mouse lung rudiments in vitro was examined by double indirect immunofluorescence microscopy. Affinity-purified monospecific polyclonal antibodies were used to examine cells after growth on glass or native collagen substrata. The data show that embryonic mesenchymal cells can produce organized fibers of type IV collagen that are not contained within a basement membrane, and that embryonic epithelial cells deposit fibers and strands of type IV collagen beneath their basal surface when grown on glass; however, when grown on a rat tail collagen substratum the epithelial cells produce a fine meshwork. To our knowledge this work represents the first report that type IV collagen can be organized by cells into a fibrous extracellular matrix that is not a basement membrane.

scholarly journals Vascular Endothelial Growth Factor Induces Endothelial Fenestrations In Vitro

1998 ◽  
Vol 140 (4) ◽  
pp. 947-959 ◽  
Author(s):  
Sybille Esser ◽  
Karen Wolburg ◽  
Hartwig Wolburg ◽  
Georg Breier ◽  
Teymuras Kurzchalia ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Choroid Plexus ◽  
Vascular Endothelial ◽  
Caveolin 1 ◽  
Endothelial Growth Factor

Abstract. Vascular endothelial growth factor (VEGF) is an important regulator of vasculogenesis, angiogenesis, and vascular permeability. In contrast to its transient expression during the formation of new blood vessels, VEGF and its receptors are continuously and highly expressed in some adult tissues, such as the kidney glomerulus and choroid plexus. This suggests that VEGF produced by the epithelial cells of these tissues might be involved in the induction or maintenance of fenestrations in adjacent endothelial cells expressing the VEGF receptors. Here we describe a defined in vitro culture system where fenestrae formation was induced in adrenal cortex capillary endothelial cells by VEGF, but not by fibroblast growth factor. A strong induction of endothelial fenestrations was observed in cocultures of endothelial cells with choroid plexus epithelial cells, or mammary epithelial cells stably transfected with cDNAs for VEGF 120 or 164, but not with untransfected cells. These results demonstrate that, in these cocultures, VEGF is sufficient to induce fenestrations in vitro. Identical results were achieved when the epithelial cells were replaced by an epithelial-derived basal lamina-type extracellular matrix, but not with collagen alone. In this defined system, VEGF-mediated induction of fenestrae was always accompanied by an increase in the number of fused diaphragmed caveolae-like vesicles. Caveolae, but not fenestrae, were labeled with a caveolin-1–specific antibody both in vivo and in vitro. VEGF stimulation led to VEGF receptor tyrosine phosphorylation, but no change in the distribution, phosphorylation, or protein level of caveolin-1 was observed. We conclude that VEGF in the presence of a basal lamina-type extracellular matrix specifically induces fenestrations in endothelial cells. This defined in vitro system will allow further study of the signaling mechanisms involved in fenestrae formation, modification of caveolae, and vascular permeability.

scholarly journals IL-33 activates tumor stroma to promote intestinal polyposis

2015 ◽  
Vol 112 (19) ◽  
pp. E2487-E2496 ◽  
Author(s):  
Rebecca L. Maywald ◽  
Stephanie K. Doerner ◽  
Luca Pastorelli ◽  
Carlo De Salvo ◽  
Susan M. Benton ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mast Cell ◽  
Growth Factors ◽  
Epithelial Cells ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Cell Activation ◽  
Intestinal Polyposis ◽  
Extracellular Matrix Components

Tumor epithelial cells develop within a microenvironment consisting of extracellular matrix, growth factors, and cytokines produced by nonepithelial stromal cells. In response to paracrine signals from tumor epithelia, stromal cells modify the microenvironment to promote tumor growth and metastasis. Here, we identify interleukin 33 (IL-33) as a regulator of tumor stromal cell activation and mediator of intestinal polyposis. In human colorectal cancer, IL-33 expression was induced in the tumor epithelium of adenomas and carcinomas, and expression of the IL-33 receptor, IL1RL1 (also referred to as IL1-R4 or ST2), localized predominantly to the stroma of adenoma and both the stroma and epithelium of carcinoma. Genetic and antibody abrogation of responsiveness to IL-33 in the ApcMin/+ mouse model of intestinal tumorigenesis inhibited proliferation, induced apoptosis, and suppressed angiogenesis in adenomatous polyps, which reduced both tumor number and size. Similar to human adenomas, IL-33 expression localized to tumor epithelial cells and expression of IL1RL1 associated with two stromal cell types, subepithelial myofibroblasts and mast cells, in ApcMin/+ polyps. In vitro, IL-33 stimulation of human subepithelial myofibroblasts induced the expression of extracellular matrix components and growth factors associated with intestinal tumor progression. IL-33 deficiency reduced mast cell accumulation in ApcMin/+ polyps and suppressed the expression of mast cell-derived proteases and cytokines known to promote polyposis. Based on these findings, we propose that IL-33 derived from the tumor epithelium promotes polyposis through the coordinated activation of stromal cells and the formation of a protumorigenic microenvironment.

scholarly journals Extracellular matrix of the human thymus: immunofluorescence studies on frozen sections and cultured epithelial cells.

1985 ◽  
Vol 33 (7) ◽  
pp. 655-664 ◽  
Author(s):  
S Berrih ◽  
W Savino ◽  
S Cohen
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Type Iv Collagen ◽  
Type I Collagen ◽  
Basement Membranes ◽  
Thymic Epithelial Cells ◽  
Perivascular Spaces ◽  
Type I ◽  
Type Iv

The immunohistochemical detection of elements of the human thymic extracellular matrix in situ and in vitro is described. In the normal thymus, the intracapsular and intraseptal fibers were strongly labeled by anti-type I collagen antiserum. Basement membranes bordering the capsule, septae, and perivascular spaces were intensely stained by anti-type IV collagen, anti-fibronectin, and anti-laminin sera. In hyperplastic myasthenia gravis thymuses, the major changes consisted of discontinuities of the basement membrane adjacent to clusters of epithelial (keratin-containing) cells, among which an unusual connective framework (densely labeled by all the antisera) was observed. In vitro, most epithelial cells were strongly labeled by antifibronectin serum and to a lesser extent by the anti-type IV collagen and anti-laminin sera. In addition, fibronectin, laminin, and type IV collagen were detected in the intercellular spaces bordering the epithelial cells in culture. Results show that thymic epithelial cells participate in the synthesis of extracellular matrix elements, which as a result of their localization and influence on epithelial cell growth, should be regarded as constitutive components of the thymic microenvironment.

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