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

We have established an in vitro system with which to examine the ability of Abelson murine leukemia virus (A-MuLV) to infect early hemopoietic progenitor cells. Blast cell colonies containing less than 100 cells were shown to contain up to 85% of cells with secondary hemopoietic colony-forming ability. Infection of cells from these blast colonies resulted in generation of transformed mast cell lines when a feeder was provided. Morphological examination of cells taken from infected cultures at various times postinfection indicated a progression of cellular differentiation to the mast cell lineage. Southern analysis on early subclones of transformed cells from two wells, using a v-abl specific probe, indicated a unique pattern of viral integration amongst subclones, suggesting that all subclones had derived from a single cell in each well. Similar results were observed with helper-free Abelson virus obtained by transfecting psi 2 cells with P160 A-MuLV proviral DNA. These data indicate that hemopoietic progenitor cells can be infected by A-MuLV and subsequently in our in vitro culture condition give rise to transformed mast cell lines.
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PMID:Blast colonies containing hemopoietic progenitor cells can give rise to Abelson virus (A-MuLV)-transformed cell lines. 244

An immature v-abl-transformed mast cell line (V3-MC) was derived from a mouse that developed systemic mastocytosis after transplantation of v-abl-infected bone marrow cells. V3-MCs injected intravenously into adult BALB/c mice infiltrated the liver, spleen, and intestine by day 6 and underwent progressive differentiation and maturation, eventually resembling indigenous mast cells. In terms of their protease content, the V3-MCs that localized in the liver and spleen differed from those in the intestine, and both differed from the cultured V3-MCs. The acquired expression of certain proteases and the loss of expression of other proteases in these tissue V3-MCs defines particular phenotypes and indicates that the differentiation and maturation of mast cell-committed progenitor cells are primarily regulated by factors in the different tissue microenvironments.
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PMID:Tissue-regulated differentiation and maturation of a v-abl-immortalized mast cell-committed progenitor. 764 91

Because in humans mast cells and basophils tend to possess nonsegmented and segmented/multi-lobular nuclei, respectively, nuclear morphology has been a major criterion for assessing the lineage of metachromatic cells of hematopoietic origin. Immature metachromatic cells with mono- and multi-lobular nuclei were both obtained when bone marrow cells from BALB/c mice were cultured for 3 weeks in the presence of interleukin-3. Analogous to the indigenous mature mast cells that reside in the peritoneal cavity and skin, both populations of in vitro-derived cells expressed the surface receptor c-kit, the chymase mouse mast cell protease (mMCP) 5, the tryptase mMCP-6, and the exopeptidase carboxypeptidase A (mMC-CPA). Immunogold electron microscopy confirmed the granule location of mMC-CPA and mMCP-6 in both populations of cells, and cytochemical analysis confirmed the presence of chymotryptic enzymes in the granules. Because mature mast cells possessing multi-lobular nuclei also were occasionally found in the skeletal muscle and jejunum of the BALB/c mouse, the V3 mouse mast cell line was used to investigate the developmental relationship of mast cells that have very different nuclear structures. After the adoptive transfer of V3 mast cells into BALB/c mice, v-abl-immortalized mast cells with mono- and multi-lobular nuclei were detected in the lymph nodes and other tissues of the mastocytosis mice that expressed c-kit, mMCP-5, mMCP-6, and mMC-CPA. These studies indicate that mouse mast cells can exhibit varied nuclear profiles. Moreover, the nuclear morphology of this cell type gives no insight as to its protease phenotype or stage of development.
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PMID:Mouse mast cells that possess segmented/multi-lobular nuclei. 920 74

Acid aspiration causes pulmonary vascular permeability and PMN sequestration. By increasing pulmonary mast cells through adoptive transfer of v-abl-transformed mast cells (V3MCs) into BALB/c mice, we now show that the greater mast cell number in the lung is associated with increased pulmonary injury.
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PMID:The presence of v-abl-transformed V3 mast cells in the lungs augments pulmonary vascular permeability to acid aspiration. 1137 27