Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mast-cell-derived mediators showed mitogenic activities on mouse-transformed epidermal cell line Pam 212 cells. These activities were eluted into the low-molecular-weight fractions below a molecular weight of 10 kD on a high performance liquid chromatography TSK 2000G column, and were partially abrogated by antihistamines or anticytokine antibodies, including anti-IL1 alpha, -IL1 beta or IL6 antibodies. Pretreatment of mast cell lines with sodium butyrate enhanced the production of these factors. Calcium ionophore or Concanavalin A (ConA) stimulated mast cells to generate factor production. These results suggest that mast-cell-derived mediators might play some role in epidermal hyperplasia seen in lichenified lesions in atopic dermatitis.
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PMID:Mast-cell-derived mediators induce epidermal cell proliferation: clue for lichenified skin lesion formation in atopic dermatitis. 142 67

The effect of cultured bone marrow cell supernatant (BMS) was studied on the proliferative response of cells of the transformed murine epidermal cell line Pam 212. Elevated DNA synthesis was found in Pam 212 cells cultured with BMS from bone marrow cells grown in spleen cell conditioned medium with concanavalin A (ConA). Pam cell proliferative activity was related to the histamine content in the culture supernatant. Neither spleen cell conditioned medium with IL1, IL2, or IL3 activity, nor ConA alone, showed any effect on Pam cell growth. A soluble mediator from the cultured bone marrow cells with mast cell characteristics was thought to be responsible for the stimulation of Pam cell growth, and Con A appeared to be a prerequisite for generation of this factor by the bone marrow cells.
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PMID:Lymphokine mediated production of an epidermal cell proliferation factor by cultured murine bone marrow cells. 350 9

Mouse-transformed epidermal cell line (Pam 212) generated the soluble mediators for promoting the growth of a mast cell line (MC9) in the presence of retinoic acid at a concentration of 10(-6)-10(-7) M. The effective molecule of MC9 cell growth promoting factor (MC9-GF) was non-dialyzable and eluted between the molecular weight of 45 K and 68 K on a TSK 2000 G column. Chromatofocusing analysis revealed that this factor had a pI range between 7.0 and 7.5. Anti-c-kit ligand antibody abrogated MC9-GF activity and RT-PCR analysis demonstrated that retinoic acid upregulates c-kit ligand mRNA expression by Pam cells. Several recombinant cytokines including IL1-alpha, IL-1 beta, IL-2, IL-3 or IL-4 did not promote MC9 cell growth at a concentration of 100 U/ml. The presence of anti-IL-1 alpha, -IL-1 beta, -IL-2, -IL-3 or -IL-4 antibodies did not abrogate the MC9-GF activity except for anti-c-kit ligand antibody.
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PMID:Retinoic acid upregulates c-kit ligand production by murine keratinocyte in vitro and increases cutaneous mast cell in vivo. 753 79

Interleukin 33 (IL33) is a recently described member of the IL1 superfamily of cytokines. Originally defined on the basis of T-cell subset differentiation, IL33 is now recognised to mediate a wider role in regulating components of the innate immune response also, particularly via mast cell activation. In this paper the basic biology of IL33 is described together with that of its cognate receptor, ST2L, and the existing knowledge base for its potential role in mediating human pathology across a range of diseases is defined.
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PMID:Role of interleukin 33 in human immunopathology. 1999 43

Sphingolipids and their synthetic enzymes are emerging as important mediators in inflammatory responses and as regulators of immune cell functions. In particular, sphingosine kinase (SK) and its product sphingosine-1-phosphate (S1P) have been extensively implicated in these processes. SK catalyzes the phosphorylation of sphingosine to S1P and exists as two isoforms, SK1 and SK2. SK1 has been shown to be activated by cytokines including tumor necrosis factor-alpha (TNF-alpha) and interleukin1-beta (IL1-beta). The activation of SK1 in this pathway has been shown to be, at least in part, required for mediating TNF-alpha and IL1-beta inflammatory responses in cells, including induction of cyclo-oxygenase 2 (COX2). In addition to their role in inflammatory signaling, SK and S1P have also been implicated in various immune cell functions including, mast cell degranulation, migration of neutrophils, and migration and maturation of lymphocytes. The involvement of sphingolipids and sphingolipid metabolizing enzymes in inflammatory signaling and immune cell functions has implicated these mediators in numerous inflammatory disease states as well. The contribution of these mediators, specifically SK1 and S1P, to inflammation and disease are discussed in this review.
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PMID:Sphingosine kinase: Role in regulation of bioactive sphingolipid mediators in inflammation. 2015 22

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 Apc(Min/+) 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 Apc(Min/+) 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 Apc(Min/+) 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.
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PMID:IL-33 activates tumor stroma to promote intestinal polyposis. 2591 79