Characterization of gene expression profiles for different types of mast cells pooled from mouse stomach subregions by an RNA amplification method

Tsuchiya, Soken; Tachida, Yuki; Segi-Nishida, Eri; Okuno, Yasushi; Tamba, Shigero; Tsujimoto, Gozoh; Tanaka, Satoshi; Sugimoto, Yukihiko

doi:10.1186/1471-2164-10-35

Cited by 15 publications

(9 citation statements)

References 42 publications

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“…It was noteworthy that a drastic downregulation of Hdc, which encodes the enzyme responsible for histamine synthesis, was unexpectedly observed (Figure 1e). We previously demonstrated that Ptgr1, which encodes the enzyme involved in inactivation of the eicosanoids, was expressed in the mucosal mast cells, not in the connective-tissue-type mast cells in murine stomach [20]. Expression of Ptgr1 was found to be moderately upregulated in our system (Figure 1f).…”

Section: Combination Of Il-9 and Scf Induced Expression Of Mcpt1 And mentioning

confidence: 52%

Establishment and Characterization of a Murine Mucosal Mast Cell Culture Model

Kakinoki

Kameo

Shoko

et al. 2019

IJMS

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Accumulating evidence suggests that mast cells play critical roles in disruption and maintenance of intestinal homeostasis, although it remains unknown how they affect the local microenvironment. Interleukin-9 (IL-9) was found to play critical roles in intestinal mast cell accumulation induced in various pathological conditions, such as parasite infection and oral allergen-induced anaphylaxis. Newly recruited intestinal mast cells trigger inflammatory responses and damage epithelial integrity through release of a wide variety of mediators including mast cell proteases. We established a novel culture model (IL-9-modified mast cells, MCs/IL-9), in which murine IL-3-dependent bone-marrow-derived cultured mast cells (BMMCs) were further cultured in the presence of stem cell factor and IL-9. In MCs/IL-9, drastic upregulation of Mcpt1 and Mcpt2 was found. Although histamine storage and tryptase activity were significantly downregulated in the presence of SCF and IL-9, this was entirely reversed when mast cells were cocultured with a murine fibroblastic cell line, Swiss 3T3. MCs/IL-9 underwent degranulation upon IgE-mediated antigen stimulation, which was found to less sensitive to lower concentrations of IgE in comparison with BMMCs. This model might be useful for investigation of the spatiotemporal changes of newly recruited intestinal mast cells.Int. J. Mol. Sci. 2020, 21, 236 2 of 13 the intestinal nematodes and local mastocytosis in epithelial layer of the gut, trachea and kidney [8][9][10]. The number of intestinal mast cells were unchanged in the gene-targeted mice lacking IL-9 or IL-9 receptor-α chain, whereas oral-antigen-induced accumulation of intestinal mast cells was impaired in these mice [11,12]. These findings indicate that IL-9 should trigger intestinal mastocytosis upon parasite infection and newly recruited mast cells should make a significant contribution towards worm expulsion. IL-9 was found to enhance stem cell factor (SCF)-mediated proliferation of murine bone-marrow-derived cultured mast cells, although IL-9 alone could not support mast cell growth and survival [13]. It remains largely unknown how transdifferentiation of intestinal mast cells should occur under the influence of IL-9 and SCF.IL-3-dependent bone-marrow-derived cultured mast cells (BMMCs) have been investigated as a useful model of murine immature mast cells. BMMCs were initially regarded as a model of mucosal mast cells, because they stored chondroitin sulphate E, rather than heparin, in their granules and had lower amounts of histamine, both being characteristic of persistent mucosal mast cells [14]. However, accumulating evidence has suggested that there are many differences among BMMCs, resident mucosal mast cells and recruited mast cells upon parasite infection. IL-3 was found to play critical roles in parasite expulsion and intestinal mastocytosis [15]. Murine mucosal mast cells recruited upon parasite infection were found to highly express a series of chymase genes, such as Mcpt1 [16], although little or no expression of the...

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Section: Combination Of Il-9 and Scf Induced Expression Of Mcpt1 And mentioning

confidence: 52%

Establishment and Characterization of a Murine Mucosal Mast Cell Culture Model

Kakinoki

Kameo

Shoko

et al. 2019

IJMS

Self Cite

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“…Cellular and extracellular matrix tissue microenvironment where mast cells are located alters mast cell responsiveness through effects on the cells by adhesive interactions . These interactions point out to biological significance of priming through cytoskeletal reorganization.…”

Section: Cytoskeleton and Mast Cell Primingmentioning

confidence: 99%

Changing the threshold—Signals and mechanisms of mast cell priming

Hálová

Rönnberg

Dráberová

et al. 2018

Immunological Reviews

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Mast cells play a key role in allergy and other inflammatory diseases involving engagement of multivalent antigen with IgE bound to high-affinity IgE receptors (FcεRIs). Aggregation of FcεRIs on mast cells initiates a cascade of signaling events that eventually lead to degranulation, secretion of leukotrienes and prostaglandins, and cytokine and chemokine production contributing to the inflammatory response. Exposure to pro-inflammatory cytokines, chemokines, bacterial and viral products, as well as some other biological products and drugs, induces mast cell transition from the basal state into a primed one, which leads to enhanced response to IgE-antigen complexes. Mast cell priming changes the threshold for antigen-mediated activation by various mechanisms, depending on the priming agent used, which alone usually do not induce mast cell degranulation. In this review, we describe the priming processes induced in mast cells by various cytokines (stem cell factor, interleukins-4, -6 and -33), chemokines, other agents acting through G protein-coupled receptors (adenosine, prostaglandin E , sphingosine-1-phosphate, and β-2-adrenergic receptor agonists), toll-like receptors, and various drugs affecting the cytoskeleton. We will review the current knowledge about the molecular mechanisms behind priming of mast cells leading to degranulation and cytokine production and discuss the biological effects of mast cell priming induced by several cytokines.

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“…Serine hydrolases may be responsible for the cinnamoyl esterase activity of the gastrointestinal mucosa; these carboxylesterases share similar structural homology and mechanism of hydrolysis with cinnamoyl esterases such as FAEA from Aspergillus niger. Serine hydrolases have been located in mast cells of the small intestine mucosa (Huntley et al, 1985), and more recently, mast cells have been characterized in the mouse stomach (Tsuchiya et al, 2009). We propose a metabolic pathway (Fig.…”

Section: Farrell Et Almentioning

confidence: 99%

Absorption and Metabolism of Chlorogenic Acids in Cultured Gastric Epithelial Monolayers

Farrell¹,

Dew²,

Poquet³

et al. 2011

Drug Metab Dispos

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ABSTRACT:Gastric absorption of feruloylquinic acid and di-O-caffeoylquinic acid analogs has never been investigated despite their potential contribution to the proposed beneficial health effects leading to reduced risk of type 2 diabetes. Using a cultured gastric epithelial model, with an acidic apical pH, the relative permeability coefficients (P app ) and metabolic fate of a series of chlorogenic acids (CGAs) were investigated. Mechanistic studies were performed in the apical to basal direction and demonstrated differential rates of absorption for different CGA subgroups. For the first time, we show intact absorption of feruloylquinic acids and caffeoylquinic acid lactones across the gastric epithelium (P app ϳ 0.2 cm/s). Transport seemed to be mainly by passive diffusion, because good linearity was observed over the incubation period and test concentrations, and we speculate that a potential carrier-mediated component may be involved in uptake of certain 4-acyl CGA isomers. In contrast, absorption of intact di-O-caffeoylquinic acids was rapid (P app ϳ 2-10 cm/s) but nonlinear with respect to time and concentration dependence, which was potentially limited by interaction with an efflux transporter and/or pH gradient dependence. For the first time, methylation is shown in gastric mucosa. Furthermore, isoferulic acid, dimethoxycinnamic acid, and ferulic acid were identified as novel gastric metabolites of CGA biotransformation. We propose that the stomach is the first location for the release of hydroxycinnamic acids, which could explain their early detection after coffee consumption.

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Characterization of gene expression profiles for different types of mast cells pooled from mouse stomach subregions by an RNA amplification method

Abstract: Background: Mast cells (MCs) play pivotal roles in allergy and innate immunity and consist of heterogenous subclasses. However, the molecular basis determining the different characteristics of these multiple MC subclasses remains unclear.

Cited by 15 publications

References 42 publications

Establishment and Characterization of a Murine Mucosal Mast Cell Culture Model

Establishment and Characterization of a Murine Mucosal Mast Cell Culture Model

Changing the threshold—Signals and mechanisms of mast cell priming

Absorption and Metabolism of Chlorogenic Acids in Cultured Gastric Epithelial Monolayers

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