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.

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 High RhoA activity maintains the undifferentiated mesenchymal cell phenotype, whereas RhoA down-regulation by laminin-2 induces smooth muscle myogenesis

2002 ◽  
Vol 156 (5) ◽  
pp. 893-903 ◽  
Author(s):  
Safedin Beqaj ◽  
Sandhya Jakkaraju ◽  
Raymond R. Mattingly ◽  
Desi Pan ◽  
Lucia Schuger
Keyword(s):  
Smooth Muscle ◽  
Serum Response Factor ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Small Gtpase ◽  
Cell Phenotype ◽  
Rhoa Activity ◽  
Functional Studies ◽  
Undifferentiated Mesenchymal Cell ◽  
Main Components

Round embryonic mesenchymal cells have the potential to differentiate into smooth muscle (SM) cells upon spreading/elongation (Yang, Y., K.C. Palmer, N. Relan, C. Diglio, and L. Schuger. 1998. Development. 125:2621–2629; Yang, Y., N.K. Relan, D.A. Przywara, and L. Schuger. 1999. Development. 126:3027–3033; Yang, Y., S. Beqaj, P. Kemp, I. Ariel, and L. Schuger. 2000. J. Clin. Invest. 106:1321–1330). In the developing lung, this process is stimulated by peribronchial accumulation of laminin (LN)-2 (Relan, N.K., Y. Yang, S. Beqaj, J.H. Miner, and L. Schuger. 1999. J. Cell Biol. 147:1341–1350). Here we show that LN-2 stimulates bronchial myogenesis by down-regulating RhoA activity. Immunohistochemistry, immunoblotting, and reverse transcriptase–PCR indicated that RhoA, a small GTPase signaling protein, is abundant in undifferentiated embryonic mesenchymal cells and that its levels decrease along with SM myogenesis. Functional studies using agonists and antagonists of RhoA activation and dominant positive and negative plasmid constructs demonstrated that high RhoA activity was required to maintain the round undifferentiated mesenchymal cell phenotype. This was in part achieved by restricting the localization of the myogenic transcription factor serum response factor (SRF) mostly to the mesenchymal cell cytoplasm. Upon spreading on LN-2 but not on other main components of the extracellular matrix, the activity and level of RhoA decreased rapidly, resulting in translocation of SRF to the nucleus. Both cell elongation and SRF translocation were prevented by overexpression of dominant positive RhoA. Once the cells underwent SM differentiation, up-regulation of RhoA activity induced rather than inhibited SM gene expression. Therefore, our studies suggest a novel mechanism whereby LN-2 and RhoA modulate SM myogenesis.

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 Host-cell interactions and innate immune response to an enteric pathogen in a human intestinal enteroid-neutrophil co-culture

2020 ◽  
Author(s):  
Jose M. Lemme-Dumit ◽  
Michele Doucet ◽  
Nicholas C. Zachos ◽  
Marcela F. Pasetti
Keyword(s):  
Epithelial Cell ◽  
Immune Responses ◽  
Enteric Pathogen ◽  
Innate Immune ◽  
Cell Interactions ◽  
Polymorphonuclear Neutrophils ◽  
Cell Phenotype ◽  
Cell Contact ◽  
Innate Immune Responses ◽  
Culture Model

AbstractPolymorphonuclear neutrophils (PMN) respond to inflammation and infection in the gut. The physical and molecular interactions between the human intestinal epithelium and PMN in the gut mucosa and their coordinated responses to enteric pathogens, are poorly understood. We have established a PMN-enteroid co-culture model consisting of human intestinal stem-cell derived enteroid monolayers and peripheral blood PMN. The model was characterized in terms of tissue structure, barrier function, cell phenotype, production of cytokines, and innate immune responses. Shigella was used as a model enteric pathogen to interrogate PMN and epithelial cell interactions and innate immunity. PMN added to the enteroid monolayers increased production of IL-8 and rapidly transmigrated across the epithelial cell layer. PMN immune phenotype was distinctly modified in the gut microenvironment via molecular signals and direct epithelial cell contact. Apical exposure to Shigella increased PMN migration and production of IL-6 by co-cultured cells. PMN became activated and efficiently phagocytosed bacteria at the apical epithelial cell surface. The co-culture model revealed PMN-epithelial cell direct communication, tissue-driven PMN phenotypic adaptation and enhancement of anti-microbial function. This novel ex vivo epithelial cell-PMN co-culture system is relevant for mechanistic interrogation of host-microbe interactions and innate immune responses and the evaluation of preventive/therapeutic tools.

scholarly journals Mesenchymal Cells Regulate Retinoic Acid Receptor-Dependent Cortical Thymic Epithelial Cell Homeostasis

2012 ◽  
Vol 188 (10) ◽  
pp. 4801-4809 ◽  
Author(s):  
Katarzyna M. Sitnik ◽  
Knut Kotarsky ◽  
Andrea J. White ◽  
William E. Jenkinson ◽  
Graham Anderson ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cell ◽  
Retinoic Acid Receptor ◽  
Mesenchymal Cells ◽  
Thymic Epithelial Cell ◽  
Cell Homeostasis ◽  
Acid Receptor

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.

scholarly journals Chicken homeobox gene Msx-1: structure, expression in limb buds and effect of retinoic acid

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 431-444 ◽  
Author(s):  
Y. Yokouchi ◽  
K. Ohsugi ◽  
H. Sasaki ◽  
A. Kuroiwa
Keyword(s):  
Retinoic Acid ◽  
Early Stage ◽  
Local Treatment ◽  
Cell Lineage ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Mirror Image ◽  
Limb Bud ◽  
Northern Analysis ◽  
Limb Buds

A chicken gene carrying a homeobox highly homologous to the Drosophila muscle segment homeobox (msh) gene was isolated and designated as Msx-1. Conceptual translation from the longest ORF gave a protein of 259 amino acids lacking the conserved hexapeptide. Northern analysis detected a single 2.6 kb transcript. As early as day 2 of incubation, the transcript was detected but was not found in adult tissue. In situ hybridization analysis revealed that Msx-1 expression is closely related to a particular mesenchymal cell lineage during limb bud formation. In early stage embryos, Msx-1 was expressed in the somatopleure. When primordial mesenchyme cells for limb bud were generated from the Wolffian ridge of the somatopleure, Msx-1 expression began to diminish in the posterior half of the limb bud then in the presumptive cartilage-forming mesenchyme. In developing limb buds, remarkable expression was seen in the apical ectodermal ridge (AER), which is responsible for the sustained outgrowth and development of the limb. The Msx-1 transcripts were found in the limb mesenchymal cells in the region covering the necrotic zone and ectodermal cells overlying such mesenchymal cells. Both ectodermal and mesenchymal expression in limb bud were rapidly suppressed by local treatment of retinoic acid which can generate mirror-image duplication of digits. This indicates that retinoic acid alters the marginal presumptive non-cartilage forming mesenchyme cell lineage through suppression of Msx-1 expression.

scholarly journals Synchronized mesenchymal cell polarization and differentiation shape the formation of the murine trachea and esophagus

2018 ◽  
Author(s):  
Keishi Kishimoto ◽  
Masaru Tamura ◽  
Michiru Nishita ◽  
Yasuhiro Minami ◽  
Akira Yamaoka ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Epithelial Cell ◽  
Progenitor Cell ◽  
Mesenchymal Cell ◽  
Cell Polarization ◽  
Radial Polarization ◽  
Cartilage Development ◽  
Tube Shape ◽  
Tube Morphogenesis

AbstractTube morphogenesis is essential for internal-organ development, yet the mechanisms regulating tube shape remain unknown. Here we show that different mechanisms regulate the length and diameter of the murine trachea. First, we found that trachea development progresses via elongation and expansion processes. In the first stage, synchronized radial polarization of smooth muscle (SM) progenitor cells with inward Golgi-apparatus displacement regulates tube elongation, controlled by mesenchymal Wnt5a–Ror2 signaling. This radial polarization directs SM progenitor cell migration toward the epithelium, and the resulting subepithelial morphogenesis supports tube elongation to the anteroposterior axis. This radial polarization also regulates esophageal elongation. Subsequently, cartilage development helps expand the tube diameter, which drives epithelial cell reshaping to determine the optimal lumen shape for efficient respiration. These findings suggest a strategy in which straight-organ tubulogenesis is driven by subepithelial cell polarization and ring cartilage development.

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

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