E-Cadherin and Cadherin-Associated Cytoplasmic Proteins Are Expressed in Murine Mast Cells

Tegoshi, Tatsuya; Nishida, Motohiro; Ishiwata, Kenji; Kobayashi, Takahiko; Uchiyama, Fukumi; Nabeshima, Kazuki; Nawa, Yukifumi; Arizono, Naoki

doi:10.1038/labinvest.3780167

Cited by 20 publications

(26 citation statements)

References 32 publications

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“…Total RNA was extracted with TRI reagent and analysed by reversetranscription polymerase chain reaction (RT-PCR) using a TITANIUM One-Step RT-PCR kit (Becton Dickinson, San Jose, CA) and previously reported forward and reverse primers for snail (Gotzmann et al, 2002), SIP1 (Cacheux et al, 2001), slug (Zhao et al, 2002), E12/E47 (Perez-Moreno et al, 2001), E-cadherin (Tegoshi et al, 2000), N-cadherin (Chung et al, 1998) and GAPDH (Xu et al, 2000). β-Actin primers were supplied with the kit.…”

Section: Conventional Rt-pcrmentioning

confidence: 99%

Cadherin switching: essential for behavioral but not morphological changes during an epithelium-to-mesenchyme transition

Maeda

Johnson

Wheelock

2005

Journal of Cell Science

362

348

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Epithelium-to-mesenchyme transitions (EMTs) are characterized by morphological and behavioral changes in cells. During an EMT, E-cadherin is downregulated while N-cadherin is upregulated. The goal of this study was to understand the role cadherin switching plays in EMT using a classical model system: transforming growth factor β1 (TGF-β1)-mediated EMT in mammary epithelial cells. We showed that stress fibers and focal adhesions are increased, and cell-cell junctions are decreased in response to TGF-β1. Moreover, these changes were reversible upon removal of TGF-β1. Downregulation of E-cadherin and upregulation of N-cadherin were both transcriptional. Neither experimental knockdown nor experimental overexpression of N-cadherin interfered with the morphological changes. In addition, the morphological changes associated with EMT preceded the downregulation of E-cadherin. Interestingly, TGF-β1-induced motility in N-cadherin-knockdown cells was significantly reduced. Together, these data suggest that cadherin switching is necessary for increased motility but is not required for the morphological changes that accompany EMT.

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Section: Conventional Rt-pcrmentioning

confidence: 99%

Cadherin switching: essential for behavioral but not morphological changes during an epithelium-to-mesenchyme transition

Maeda

Johnson

Wheelock

2005

Journal of Cell Science

362

348

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“…12,13 PMCs (2000 cells/well) were allowed to adhere to coated wells of a 96-well plate for 1 hour at 37°C. Wells were coated with either BSA (0.5 mg/mL), collagen type I (rat tail, 25 g/mL; BD Biosciences), or fibronectin (bovine plasma, Sigma-Aldrich, 25 g/mL).…”

Section: In Vitro Mast Cell Adhesionmentioning

confidence: 99%

Mast cell–mediated inflammatory responses require the α2β1 integrin

Edelson

Pappan

et al. 2004

Blood

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Although the ␣2␤1 integrin is widely expressed and has been extensively studied, it has not been previously implicated in mast cell biology. We observed that ␣2 integrin subunit-deficient mice exhibited markedly diminished neutrophil and interleukin-6 responses during Listeria monocytogenes-and zymosan-induced peritonitis. Since exudative neutrophils of wildtype mice expressed little ␣2␤1 integrin, it seemed unlikely that this integrin mediated neutrophil migration directly. Here, we demonstrate constitutive ␣2␤1 integrin expression on peritoneal mast cells. Although ␣2-null mice contain normal numbers of peritoneal mast cells, these ␣2-null cells do not support in vivo mast cell-dependent inflammatory responses.We conclude that ␣2␤1 integrin provides a costimulatory function required for mast cell activation and cytokine production in response to infection. IntroductionThe ␣2␤1 integrin, a receptor for collagen, laminin, and other nonmatrix ligands, is expressed on a number of distinct cell types including epithelial cells, endothelial cells, fibroblasts, platelets, and leukocytes. 1 On cells of the immune system, the ␣2␤1 integrin is expressed on a subset of activated T lymphocytes (hence the designation very late activation antigen-2), on natural killer (NK) cells (DX5, originally defined as an NK cell-specific marker, was recently shown to recognize the ␣2␤1 integrin), and on neutrophils (polymorphonuclear leukocytes [PMNs]). 2,3 Although the role of the ␣2␤1 integrin in immune regulation is poorly understood, accumulating evidence suggests that this integrin may play an important role in leukocyte adhesion and extravasation from the vasculature into peripheral tissues. [4][5][6] Recently, we generated an ␣2 integrin subunit-deficient mouse model to investigate the role of the ␣2␤1 integrin in normal development and the pathogenesis of disease. 7 Here, we report that the ␣2 integrin-deficient mouse demonstrates a profound and surprising defect in the innate immune response during acute peritonitis. ␣2 integrin-deficient mice exhibit markedly diminished inflammatory responses to both Listeria monocytogenes, a gram-positive bacterium, and zymosan, a fungal polysaccharide. Although the PMNs of the ␣2 integrin-deficient mouse lack expression of this integrin, the inflammatory defect in these mice is not due to an inability of the PMNs to extravasate into the peritoneum. Instead, the ␣2␤1 integrin is expressed at high levels on all peritoneal mast cells (PMCs), a cell type required for the induction of the inflammatory response to infection. 8,9 We demonstrate that ␣2␤1 integrin expression on the PMC is required for mast cell activation and cytokine release in response to a number of agents in vivo and that ␣2␤1 integrin expression on the PMC is necessary for induction of normal inflammatory responses. Materials and methods Mice␣2 integrin-deficient mice on a C57BL/6 ϫ 129/Sv background were used at 6 to 20 weeks of age, with wild-type littermate controls. 7 Mice were maintained and bred under specific pathogen-...

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“…It was shown that E-and N-cadherins, a-and b-catenins, and p120 catenin were expressed in BMMC, and that E-cadherin and associated cytoplasmic proteins might be involved in the regulation of certain stage of mast cell differentiation and cell-cell interactions. 13) However, it was unclear until now whether cadherins and/or associated proteins were concerned in the contacts between neurites and mast cells. The present experiments indicated that both N-cadherin and E-cadherin in BMMC were spread over in the cytoplasm of BMMC without association of the neurites.…”

mentioning

confidence: 99%

N-Cadherin Plays a Role in the Synapse-Like Structures between Mast Cells and Neurites

Suzuki

Furuno

et al. 2004

Biological & Pharmaceutical Bulletin

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During the last decade there has been an exponential increase in data illustrating that the nervous and immune systems are not disparate entities.1,2) The nerve-mast cell relationship has served as a prototypic association and has provided substantial evidence for bi-directional communication between nerves and immune cells.3) Early studies elegantly described the non-random spatial association of nerves and mast cells in a variety of tissues in which actual membrane-membrane contacts could be observed. 4,5) To understand these events we have studied recently direct neurite-mast cell (RBL) communication using an in vitro co-culture approach and a calcium imaging by confocal laser scanning microscopy (CLSM). Our results showed clearly that nerve-mast cell communication can occur in the absence of an intermediary transducing cell and that the neuropeptide substance P, operating via NK-1 receptors, is an important mediator of this communication.6) Our findings have implications for the neuroimmune signaling cascade that are likely to occur during airways inflammation, intestinal hypersensitivity, and other conditions in which mast cells feature. [6][7][8] In addition we studied by atomic force microscopy (AFM) the morphological structure of the interaction between neurites and mast cells (RBL) which was involved in the communication.9) AFM images showed that association between the growth cone of neurites and the RBL cell occurred over ca. 7 mm and that direct neurite-mast cell cross-talk induced degranulation in RBL cells via the neuropeptide substance P.In the present paper we have focused on the molecular mechanism of the membrane proteins involved in the synapse-like structure between neurites and mast cells. We used an in vitro co-culture approach comprising superior cervical ganglia (SCG) and mouse bone marrow-derived mast cells (BMMC) besides RBL cells. Mast cells are classified into two types. One is mucosal and another is connective tissue type. Both RBL cells and BMMCs belong to mucosal type mast cells. However, RBL cells are much more adhesive than BMMCs and would like to non-specifically stick to the supported matrigel-coated plate of glass dishes. They also have a malignant feature. In addition, nerves most commonly associated with mast cells in vivo contain substance P.5) Substance P in isolated neurons from SCG maintained in culture showed a 25-fold increase within 48 h in vitro.10) Therefore, we studied an in vitro co-culture approach comprising SCG and BMMC to understand precisely adhesion proteins that play a role in the neurite-mast cell communication.Cadherins are a family of calcium-dependent and homophilic cell adhesion proteins that play in the formation of synaptic plasticity. E-and N-cadherins, which are classic cadherins, are found in synapses and they appear to straddle the presynaptic and postsynaptic membranes surrounding the active zone and the postsynaptic density.11) Cadherins mediate strong adhesion through intracellular interaction with b-catenin, which in turn associates with a-ca...

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E-Cadherin and Cadherin-Associated Cytoplasmic Proteins Are Expressed in Murine Mast Cells

Cited by 20 publications

References 32 publications

Cadherin switching: essential for behavioral but not morphological changes during an epithelium-to-mesenchyme transition

Cadherin switching: essential for behavioral but not morphological changes during an epithelium-to-mesenchyme transition

Mast cell–mediated inflammatory responses require the α2β1 integrin

N-Cadherin Plays a Role in the Synapse-Like Structures between Mast Cells and Neurites

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