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At least 163 records · Page 9Linked to original sources
PubMed2000

Interferon-mediated block in cell cycle and altered integrin expression in a differentiated salivary gland cell line (HSG) cultured on Matrigel.

Sjögren's syndrome (SS), an idiopathic, autoimmune exocrinopathy, is partly characterized by diminished salivary flow, acinar cell atrophy, and increased expression of several cytokines. Several in vivo characteristics of the sialoadenitis are also evident in a human salivary gland ductal epithelial cell line (HSG) treated with cytokines. HSG cells differentiate to the acinar phenotype when cultured on Matrigel (Becton Dickinson, Bedford, MA), a basement membrane extract. To elucidate mechanisms of salivary gland pathology, the effects of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) on cell cycle progression and integrin expression were evaluated in HSG acinarlike cells. Flow cytometry experiments showed that cytokine treatment for 2 days arrested cells in G(1) phase of the cell cycle, and this preceded significant morphologic changes and decreased viability. Whereas only modest cytokine-mediated increases in protein expression for the alpha 3 and beta 1 integrin subunits were seen by immunoprecipitation, a form of alpha 3 integrin displaying enhanced electrophoretic mobility was evident after 6 days of cytokine treatment. To our knowledge, this is the first report demonstrating an IFN-mediated alteration in the electrophoretic mobility of integrin subunits. From this study, it was evident that the combination of IFN-gamma and TNF-alpha resulted in a block in G(1) phase for acinar cells before accumulation of the alpha 3 integrin variant or significant degenerative cellular changes. Information from the present and previous studies suggests that cytokines may alter the pattern of integrin expression and block cell cycle progression in salivary gland cells grown in three-dimensional acinarlike clusters. These experiments may provide a new cell culture model to study the effects of cytokines in normal and diseased salivary glands, including SS.

Antigens, CD↗
PubMed2006

Contact with existing adipose tissue is inductive for adipogenesis in matrigel.

The effect of adipose tissue on inductive adipogenesis within Matrigel (BD Biosciences) was assessed by using a murine chamber model containing a vascular pedicle. Three-chamber configurations that varied in the access to an adipose tissue source were used, including sealed- and open-chamber groups that had no access and limited access, respectively, to the surrounding adipose tissue, and a sealed-chamber group in which adipose tissue was placed as an autograft. All groups showed neovascularization, but varied in the amount of adipogenesis seen in direct relation to their access to preexisting adipose tissue: open chambers showed strong adipogenesis, whereas the sealed chambers had little or no adipose tissue; adipogenesis was restored in the autograft chamber group that contained 2- to 5-mg fat autografts. These showed significantly more adipogenesis than the sealed chambers with no autograft ( p < 0.01). Autografts with 1mg of fat were capable of producing adipogenesis but did so less consistently than the larger autografts. These findings have important implications for adipose tissue engineering strategies and for understanding de novo production of adipose tissue.

Adipogenesis↗
PubMed1994

In vitro interactions of endometrial stromal and epithelial cells in Matrigel: reorganization of the extracellular matrix.

Fragments of human endometrial glands and dispersed endometrial stromal cells were cultured together in a thick layer of reconstituted basement membrane (Matrigel). Epithelial cells kept their glandular morphology whereas stromal cells grew into round clusters of mainly fusiform cells. Transmission electron micrographs showed collagen fibers between stromal cells as well as in surrounding extracellular matrix after 2.5 weeks. A well-defined basement membrane was found when epithelial and stromal cells were in close proximity to each other. Beneath the lamina densa there was a loose network of collagen fibers or a dense fibrillar network arranged parallel to the cell layers. Epithelial cells showed hemidesmosomes at their basal surface where they were close to stromal cells.

Cell Communication↗
PubMed2004

Both mitogen activated protein kinase and the mammalian target of rapamycin modulate the development of functional renal proximal tubules in matrigel.

Tubules may arise during branching morphogenesis through several mechanisms including wrapping, budding, cavitation and cord hollowing. In this report we present evidence that is consistent with renal proximal tubule formation through a process of cord hollowing (a process that requires the concomitant establishment of apicobasal polarity and lumen formation). Pockets of lumen filled with Lucifer Yellow were observed within developing cords of rabbit renal proximal tubule cells in matrigel. The observation of Lucifer Yellow accumulation suggests functional polarization. In the renal proximal tubule Lucifer Yellow is initially transported intracellularly by means of a basolaterally oriented p-aminohippurate transport system, followed by apical secretion into the lumen of the nephron. Consistent with such polarization in developing tubules, Triticum vulgare was observed to bind to the lumenal membranes within pockets of Lucifer Yellow-filled lumens. As this lectin binds apically in the rabbit renal proximal tubule, T. vulgare binding is indicative of the emergence of an apical domain before the formation of a contiguous lumen. Both epidermal growth factor and hepatocyte growth factor stimulated the formation of transporting tubules. The stimulatory effect of both epidermal growth factor and hepatocyte growth factor on tubulogenesis was inhibited by PD98059, a mitogen activated protein kinase kinase inhibitor, rather than by wortmannin, an inhibitor of phosphoinositide 3-kinase. Nevertheless, Lucifer Yellow-filled lumens were observed in tubules that formed in the presence of PD98059 as well as with wortmannin, indicating that these drugs did not prevent the process of cavitation. By contrast, rapamycin, an inhibitor of the mammalian target of rapamycin, prevented the process of cavitation without affecting the frequency of formation of developing cords. Multicellular cysts were observed to form in 8-bromocyclic AMP-treated cultures. As these cysts did not similarly accumulate Lucifer Yellow lumenally, it is very likely that processes other than organic anion accumulation are involved in the process of cystogenesis, including the Na,K-ATPase.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

The role of S100A4 gene encoding an S100-related calcium-binding protein in human bile duct adenocarcinoma cell lines: correlation of S100A4 expression and invasive growth in Matrigel Matrix.

S100A4, one of the tandemly arranged S100 genes at chromosome 1q21, has been suggested to play a functional role in cell motility and invasiveness of tumor cell growth. We investigated the expression of S100A4 and the in vitro invasiveness of 4 human bile duct adenocarcinoma cell lines by the Matrigel assay. S100A4 was abundantly expressed in 2 adenocarcinoma cell lines whose growth pattern was highly invasive. Induction of antisense S100A4 into one of the cell lines decreased S100A4 mRNA levels and reduced invasiveness. In contrast, induction of sense S100A4 expression into non-invasive KMBC adenocarcinoma cells, which originally lacked S100A4 expression, resulted in apparent invasive potential in the transfected cells compared with the cells with the vector alone. These results suggest that S100A4 expression is well correlated with the invasiveness of human bile duct adenocarcinomas.

Adenocarcinoma↗
PubMed2004

HOXA10 regulates p53 expression and matrigel invasion in human breast cancer cells.

HOX genes regulate cell differentiation during embryonic development. Here we demonstrate HOXA10 expression in both benign and malignant adult human breast tissue and in MCF-7, but not BT20 breast cancer cells. We have previously shown that HOXA10 mediates uterine differentiation in response to estrogens. The mechanism of action of estradiol and other estrogen receptor modulators on breast cancer cell growth is still poorly understood. MCF-7 cells, which are ER (+) and express HOXA10, were used to assay the effect of estradiol and tamoxifen on HOXA10 expression. Semi-quantitative RT-PCR and northern analysis revealed that treatment with either estradiol or tamoxifen increased HOXA10 mRNA expression. BT20 cells, which are ER (-) and do not endogenously express HOXA10, were used to assay the effect of increased HOXA10 expression on p53 expression and on the invasive phenotype. Constitutively expressing HOXA10 in BT20 cells increased p53 protein expression. Increased HOXA10 also reduced invasiveness through matrigel. The mechanism by which estrogen and other estrogen receptor modulators influence both normal breast development as well as breast cancer may involve the regulation of developmental control genes such as HOXA10; HOXA10 in turn regulates expression of key downstream genes such as p53 and regulates tumor cell functional phenotype.

Adult↗
PubMedDate not supplied

Kepone (chlordecone) disrupts adherens junctions in human breast epithelial cells cultured on matrigel.

Perturbations in cell-extracellular matrix (ECM) interactions are a consistent feature of mammary tumors and cells in culture. We have utilized MCF-10ATG3B human breast epithelial cells to examine whether the organochlorine Kepone induces alterations in cell adhesion molecules important to cell-cell and cell-ECM interactions. Kepone effects on the levels and association of proteins involved in adherens junctions or desmosomes were examined using immunoblot analysis and immunoprecipitation. MCF-10ATG3B cells cultured on an ECM of Matrigel form lattice-like structures that are disrupted with 0.1 and 1 microM Kepone. E-cadherin protein levels decreased significantly by approximately 23% and approximately 69% following treatment with 0.1 and 1.0 microM Kepone, respectively, relative to solvent-treated cells. Desmoglein and alpha- and gamma-catenin levels did not vary significantly with Kepone. Beta-catenin protein levels decreased significantly by approximately 37%, 36% and 53% at 0.01, 0.1 and 1.0 microM Kepone, respectively. E-cadherin-gamma-catenin association was disrupted with 0.1 and 1.0 microM Kepone. Thus, Kepone disrupts cellular architecture, specifically E-cadherin-gamma-catenin containing adherens junctions, which may ultimately affect cellular phenotype.

Adherens Junctions↗
PubMed2001

Experimental prostate epithelial morphogenesis in response to stroma and three-dimensional matrigel culture.

To reproduce the structural and functional differentiation of human prostatic acini in vivo, prostatic epithelial and stromal cells derived from human primary cultures were cocultured in Matrigel. In the absence of stroma and serum, epithelial spheroids composed of solid masses of stratified and cuboidal cells formed. Outer cells of the spheroid expressed cytokeratins 1, 5, 10, and 14, whereas the inner cells expressed cytokeratin 18. The addition of 2% serum induced formation of a lumen surrounded by a layer of one or two cuboidal and columnar epithelial cells. The further addition of stromal cultures, dihydrotestosterone, and estrogen induced polarization of the epithelium and increased spheroid-forming efficiency. Epithelium expressed either cytokeratin 18 alone or additionally cytokeratins 1, 5, 14, and 10. All spheroid epithelium expressed prostate-specific antigen and prostate-specific membrane antigen. Androgen receptor was only detected in the presence of stroma, serum, and hormones. Thus, development of a functional and morphologically correct prostate gland in vitro is dependent on extracellular matrix, steroid hormones, and factors from stromal cells and serum.

Animals↗
PubMed1991

Effects of synthetic peptides and protease inhibitors on the interaction of a human ovarian cancer cell line (NIH:OVCAR-3) with a reconstituted basement membrane (Matrigel).

We have investigated the adhesive properties and invasiveness of cells of the human ovarian carcinoma line, NIH:OVCAR-3, in vitro. OVCAR-3 cells exhibited a similar rate of adhesion to all substrates tested including laminin, fibronectin, and collagens I and IV. The synthetic peptide YIGSR-NH2, which corresponds to an attachment site in laminin, inhibited the adhesion of the cells to laminin, but not to fibronectin. In contrast, a GRGDS-NH2 peptide blocked adhesion to fibronectin but not to laminin. OVCAR-3 cells invaded and formed branched colonies on Matrigel. Colony formation was retarded by both YIGSR-NH2 and GRGDS-NH2 peptides. Serine protease inhibitors and human recombinant TIMP, the tissue inhibitor of metalloproteases, inhibited ovarian tumor cell invasion while a synthetic collagenase IV inhibitor (SC-44463) had no effect. These studies suggest that metalloproteases other than collagenase IV may be important for the invasive activity of ovarian cancer cells. It is possible that synthetic peptides with antiadhesive cellular activity and certain antiproteases could be used to control the progressive colonization and invasion of peritoneal surfaces by malignant ovarian cancer cells.

Amides↗
PubMed1993

Effect of Matrigel and laminin peptide YIGSR on tumor growth and metastasis.

Basement membrane has a variety of effects on tumor cells and promotes malignant behavior. Tumor cell growth is enhanced both in vitro and in vivo in mice in the presence of basement membrane. This has led to the ability to grow various tumors including human biopsy specimens in nude mice. Furthermore, low cell numbers can be used when coinjected with Matrigel, a basement membrane extract. The basement membrane glycoprotein laminin is important in promoting invasive behavior and the level of a 32/67 kDa laminin receptor has been shown to correlate with malignancy. A sequence of five amino acids, tyrosine-isoleucine-glycine-serine-arginine (YIGSR) has been shown to recognize this receptor and to reduce experimental metastases (tail vein injection resulting in colonization of the lung) and subcutaneous tumor growth. This peptide is active in both models either when coinjected or when daily intraperitoneal injections are given after tumor growth has initiated. YIGSR does not effect cell arrest but does inhibit angiogenesis which is necessary for tumor growth. YIGSR also appears to have an additional antitumor effect via its interaction with a specific receptor. YIGSR-adherent cells established after 30 successive selections on YIGSR-coated dishes in vitro formed more lung colonies after intravenous injection and larger tumors after subcutaneous injection than the parent B16F10 melanoma cells. The YIGSR-non-adherent cells formed fewer lung colonies and smaller subcutaneous tumors. These data demonstrate the importance of laminin-tumor cell interactions in malignancies and suggest that a short sequence from laminin has multiple effects in reducing tumor growth and spread.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMedDate not supplied

Ultrastructure of interactions between activated murine natural killer cells and melanoma cells in an extracellular matrix (Matrigel) environment.

Mixed suspensions of B16-F10 melanoma cells and murine interleukin 2 (IL2)-activated (adherent) natural killer (A-NK) cells cultured for 5 days were enclosed in gelled droplets of reconstituted basement membrane extracellular matrix (Matrigel). After incubation under cell culture conditions +/- IL2, samples were fixed for electron microscopy after 10 min and 2, 6, and 24 h. At the first time point cells were rounded and randomly distributed in the gel, at 2 h A-NK cells migrated vividly and formed contacts with target cells. At 6 h there were extensive effector:target conjugates and melanoma cell debris in the gel. Directed exocytosis of A-NK cell-specific granules could not be verified. At 24 h very few intact B16 cells remained in IL2-substituted specimens and there were large amounts of lytic melanoma cell remnants; in the absence of IL2 substantial numbers of surviving melanoma cells formed aggregates. At this time some A-NK cells had ingested melanoma cell components which probably fused with specific two-compartment granules to form large phagolysosomes. A-NK cells enlarged into a giant cell type with huge cytoplasmic accumulations of amorphous material described as mucoid masses by others.

Animals↗
PubMed1997

Alpha-melanocyte-stimulating hormone blocks invasion of reconstituted basement membrane (Matrigel) by murine B16 melanoma cells.

We have examined the effect of alpha-melanocyte-stimulating hormone (alpha-MSH) on invasive ability of murine melanoma cell lines with different metastatic potential in a Matrigel invasion assay. alpha-MSH potently blocked the invasion of B16-BL6 cells with highly metastatic potential in a concentration-dependent manner, whereas it was less effective in inhibiting the invasion of weakly metastatic B16-F1 cells. Pretreatment of B16-BL6 cells with alpha-MSH resulted in a decrease of the adhesiveness to fibronectin and laminin substrates in a time-dependent fashion. As assessed by zymographic analysis, alpha-MSH partially inhibited the production of matrix metalloproteinase (MMP)-2 and -9 from both cell lines to a similar degree without affecting the degradative activity of these MMPs. alpha-MSH was more potent in inhibiting the migration of B16-BL6 cells towards both fibronectin- and laminin-coated substrates than that of B16-F1 cells. The growth and morphology of B16-BL6 cells were not changed after a 7-day incubation with alpha-MSH. The number of lung tumor colonies markedly decreased when B16-BL6 cells were coinjected intravenously with 10(-6) M alpha-MSH. However, alpha-MSH had no effect on the experimental lung metastases by B16-F1 cells. These results suggest that alpha-MSH suppressed the invasive and metastatic properties of B16 melanoma cells, and the degree of inhibition was associated with metastatic potential of B16 melanoma cells.

Animals↗
PubMed1993

Effects of fatty acids on invasion through reconstituted basement membrane ('Matrigel') by a human breast cancer cell line.

An in vitro invasion assay system was used to examine the effects of linoleic acid, an omega-6 fatty acid, and two omega-3 fatty acids, eicosapentaenoic acid and docosahexaenoic acid, on the invasive capacity of MDA-MB-435 human breast cancer cells. Linoleic acid stimulated, and the omega-3 fatty acids inhibited, tumor cell invasion at concentrations of 0.25 and 0.5 microgram/ml. Indomethacin, 20 micrograms/ml, completely suppressed the stimulatory activity of linoleic acid, suggesting that these fatty acid effects are mediated via eicosanoid biosynthesis.

Analysis of Variance↗
PubMed1994

Regulation of cytochrome P450 2B1/2 mRNAs by Kepone (chlordecone) and potent estrogens in primary cultures of adult rat hepatocytes on Matrigel.

We previously reported that when primary cultures of rat hepatocytes were treated with phenobarbital (PB) or one of several organochlorine pesticides, including Mirex, there was co-induction of cytochrome P450 2B1 and 2B2 mRNAs and immunoreactive proteins, whereas Kepone selectively induced 2B2 (Kocarek et al. (1991) Mol. Pharmacol. 40, 203-210). Indeed, Kepone treatment actively suppressed induction of 2B1 and 2B2 mRNAs in hepatocytes cotreated with phenobarbital. Because Kepone differs chemically from Mirex only in the replacement of 2 chlorine atoms with a ketone group, which exists in aqueous solution as a gem-diol and appears to confer weak estrogenic properties, we treated hepatocyte cultures with one of 3 potent estrogens, beta-estradiol, 17 alpha-ethinylestradiol or diethylstilbestrol. Treatment with each of these estrogens induced 2B1 and 2B2 mRNA only at very high doses (10(-4) M). Beta-Estradiol (10(-4) M) treatment also induced 2B1/2 mRNA in hepatocyte cultures prepared from a prepubescent female rat. The anti-estrogen tamoxifen failed to reverse 2B1/2 mRNA induction following beta-estradiol or Kepone treatment of adult hepatocyte cultures. High doses of beta-estradiol or 17 alpha-ethinylestradiol failed to induce 2B1/2 mRNA in treated rats. We also examined the effects of chloral hydrate, a simple gem-diol, on 2B1/2 mRNA induction in the hepatocyte cultures. Treatment with chloral hydrate (3 x 10(-3) M), like Kepone (10(-5) M), suppressed 2B1/2 mRNA induction following phenobarbital (10(-4) M) treatment, while Kepone alcohol (10(-5) M), which is not a gem-diol, produced less suppression. Our results suggest that selective induction by Kepone of 2B2 is unlikely related to its effects as a weak classical estrogen, while the ability of Kepone to suppress induction of 2B1 and 2B2 by PB may be related to its properties as a gem-diol.

Animals↗