Local Mitogenic Effect of Tissue Mast Cell Secretion (original) (raw)
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Evidence of mast-cell histamine being mitogenic in intact tissue
Agents and Actions, 1985
In cultured rat mesentery there was a spontaneous release of about 45% of the histamine in 2 days, and a spontaneous marked increase in basal proliferation of the mesentery. The MC secretagogues, compound 48/80 and polymyxin B, released additional histamine and stimulated mitogenesis further. In contrast, 48/80 added to cultures of guinea-pig mesentery, the MC of which are unresponsive to the drug, did not affect the basal proliferation. However, exogenous histamine at 10 10 Mmitogenlcally stimulated the cultured guinea-pig mesentery. A histamine H2-reeeptor antagonist, which itself was mitogenieaUy inert, significantly suppressed the 48/80-1nduced MC-mediated mitogenesis in rat mesentery in vDo and in vitro. On the other hand, a histamine Hi-receptor antagonist did not affect this MCmediated mitogenesis in rat.
Virchows Archiv. B, Cell pathology including molecular pathology, 1981
Histamine release from tissue-bound mast cells and cell proliferation in the proper mesentery in the intact rat was quantitated following in intraperitoneal injection of graded doses of compound 48/80. The dose-response curves were sigmoid-like in linear-log plots. ED50 for histamine release was 0.035-0.040 and for increased cell proliferation 0.040-0.048 microgram per g BW. The proliferative response following mast-cell secretion ceased after a period of between 48-72 h, irrespective of whether a high or a low dose of 48/80 was used. Basal on the net rate of histamine synthesis (ca. 0.45 microgram/g mesentery wet weight/h) after an initial injection of 48/80, on the extent of histamine release and the proliferative response after a repeated injection of 48/80, it is concluded that there is a lag period of at least 3 days before proliferation can be re-stimulated by renewed 48/80-induced mast-cell secretion.
The isolation and some properties of of guinea pig mesenteric mast cells
Experimental Cell Research, 1973
A technique is described for obtaining isolated mast cells from guinea-pig mesentery by an enzymatic digestion process using hyaluronidase and collagenase. One to 4 x lo5 mast cells were obtained from the mesentery of each animal. Isolated mast cells from guinea-pigs of about 400 g were approximately spherical with a mean diameter of 6.1 pm and a mean histamine content of 8.8 pg. Studies on isolated mast cells from sensitised animals showed that the cells were still capable of an anaphylactic release of histamine when challenged with the appropriate antigen. Isolated mast cells did not sensitise when incubated with antibody dissolved in physiological saline but sometimes became weakly sensitised when incubated with the same antibody in isotonic-buffered glucose. Mast cells were found to survive in culture but they were no longer capable of an antigen-induced histamine release.
Mast Cell Degranulation and Histamine Release Observed in a New in Vitro System
Journal of Experimental Medicine, 1960
Mast cells participate in some types of inflammatory reactions involving changes in the microcirculation of certain tissues. Among the known vasoactive substances of importance, histamine has been found in mast cells (1) of several species of animals and in certain species serotonin is also present (2). A variety of substances (the formaldehyde polymer of p-methoxyphenethylmethylamine (48/80), ovomucoid, and dextran) when administered to the rat elicit an inflammatory response, cause histamine and serotonin release and the morphological change of degranulation . No clear description of the process involved in release of the active amines and other mast cell constituents has yet been presented. A major obstacle has been the lack of an appropriate way of observing the action of various agents on the structure of the mast cell and its constituents under controlled conditions. Hence, a new method of observation was sought to study the mechanism of mast cell secretion in vitro.
Mast Cell Degranulation and Parenchymal Cell Injury in the Rat Mesentery
Microcirculation, 1999
Objective: The objective of this study was to explore the degree of parenchymal cell injury after mast cell degranulation by application of compound 48/80 (CMP 48/80) in the absence of adherent leukocytes in the rat mesentery. Methods: Rats were rendered leukopenic by injection of an antibody against leukocytes, and the mesentery was superfused with CMP 48/80 during intravital microscopy. The extent of cell injury was determined using a fluorescent cellviability indicator, propidium iodide (PI). In an additional group, mast cell degranulation with CMP 48/80 was prevented by using the mast cell stabilizer Ketotifen. Results: After a reduction in the number of circulating leukocytes, mast cell degranulation produced a mild increase in parenchymal cell injury. The injury levels significantly increased when individual regions of the mesentery were compared. Stabilization of the mast cells with Ketotifen reduced the injury to below baseline values. Conclusions: In the absence of leukocyte adhesion to the endothelium, mast cell degranulation contributes to parenchymal cell injury in the mesentery.
Characterization of rat tissue cultured mast cells
European Journal of Immunology, 1990
Twelve continuous rat tissue cultured mast cell (MC) lines were established by prolonged culture of rat peritoneal MC in the absence of added factors or feeder layers. Two of these lines, RCMCl and RCMC2, have been briefly described previously, seven others are now also described. Both RCMCl and RCMC2 lack a marker chromosomes present on RBL-CA10.7 cells. All lines were found to express the phenotype of mucosal MC as defined by alcian blue-positive and safranin 0-negative staining, the presence of rat MC protease I1 and a low histamine content. When analyzed for high-(FcsRI) and low-affinity (FcsRL) receptors for IgE, the various lines yielded a variety of receptor patterns. Northern blot analysis of the RNA of RCMCl, RCMC2 and RBL-CA10.7 revealed that all three cell lines contained the same mRNA species for the a , p and y subunits for FcsRI previously found in another rat basophilic leukemia cell line. Quantitation of the relative amounts of a , p and y mRNA did not correlate with the expression of the relative amounts of FceRI(a) in these cells.The relative amounts of mRNA for all these subunits of RCMC2 were equal or higher than those of RCMCl, suggesting that the low expression of FcsRI(a) on the former was a consequence of post-transcriptional events. Analysis of a RCMCl clone over a 6-month period revealed changes in the expression of both FceRI(a) and FCERL. Abbreviations: MC: Mast cell CTMC: Connective tissue MC FcERI: High-affinity receptor for IgE FCERL: Low-affinity receptor for IgE, previously named H or FcERII. The latter designation was discontinued to avoid confusion with FcERII or CD23 found on B cells MMC: Mucosal MC RBL: Rat basophilic leukemia RCMC: Rat tissue cultured MC RMCP: Rat MC protease R(M)pMC: Rat (mouse) peritoneal MC TfR: Transferrin receptor 0 VCH Verlagsgesellschaft mbH, D-6940 Weinheim, 1990
Molecular aspects of mast-cell-mediated mitogenesis in fibroblasts and mesothelial cells in situ
Virchows Archiv. B, Cell pathology including molecular pathology, 1988
Mast-cell-mediated mitogenesis in intact tissues is a paracrine reaction the molecular mechanisms of which still have to be elucidated. One strategy worth exploring is to study the mitogenic reaction under as defined conditions as possible. The present study demonstrates that in the virtually avascular rat mesentery, organ-cultured in a biochemically-defined medium, activation of mast cells induced a mitogenic reaction in fibroblasts and mesothelial cells, the two predominant, morphologically distinct neighboring cell types. Thus the system provides a means of studying the influence of defined molecules in the growth medium on the outcome of a mitogenic response in these two cell types in situ. It was further observed that exogenous platelet-derived growth factor (PDGF) was not essential for this mast-cell-mediated mitogenic reaction to occur in the tissue-bound fibroblasts and mesothelial cells.
Mast Cells: Function and Dysfunction
Allergy and Asthma Proceedings, 1982
Mast cell (Me) degranulation, and the concomittant release of amines and other "mediators," are difficult to rationalize when they result in overt pathology, let alone in occasional death. It has been suggested that these untoward reactions represent unbridled MC function. I do not accept that view, for it rests on questionable data and it denies numerous observations that support a contrary interpretation. This is not to deny the realty of degranulation which is, of course, of major clinical concern. Research on the mechanism of degranulation is clearly of prime importance; it has been abundant, some inspired, some elegant, and so pertinent as to have eclipsed all other aspects of MC behavior. Without denigrating that effort, the present essay focuses on those other aspects and examines the role(s) MCs might play in normal physiology. I suggest that degranulation is incompatible with MC function because the granules function in situ. These statements rest in part on the following facts: I. Mast cells are small in newborn animals, but grow ever larger as the animal ages. This is referable to an'accumulation of cytoplasmic granules and at the very least, evidence that granules are not secreted as rapidly as elaborated. 2. The tinctorial characteristics of MC granules evolve over a matter of weeks, which suggests a low turnover.
Differentiation and proliferation of embryonic mast cells of the rat
The Journal of Cell Biology
Histochemical reactions and radioautography were used to investigate the sequence of mast cell development in rat embryos. Mast cells arise ubiquitously in and are confined to the loose connective tissue in the embryo. The alcian blue--safranin reaction distinguishes between weakly sulfated and strongly sulfated mucopolysaccharides by a shift from alcian blue to safranin staining. Based on this reaction and morphologic characteristics, four stages were identified. Stage I mast cells are lymphocyte-like cells with cytoplasmic granules which invariably stain blue with the alcian blue-safranin reaction. In Stage II cells the majority of granules are alcian blue-positive, but some safranin-positive granules have appeared. Stage III mast cells are distinguished by a majority of safranin-positive cytoplasmic granules; some alcian blue-posltive granules still remain. Stage IV cells contain only safranin-positive granules. Thymidine-H 3 uptake and identification of mitotic figures indicates that mast cells in Stages I and II comprise a mitotic pool while those in Stages III and IV are mitotically inactive. The pattern of $3~)4 incorporation and the sequence of appearance of histochemically identifiable mast cell constituents corroborates division of the proliferation and differentiation of embryonic mast cells into the four stages described above. The process of formation of mast cell granules is interpreted as reflecting the synthesis and accumulation of a heparin precursor in alcian blue positive granules followed by the synthesis and accumulation of highly N-sulfated heparin along with mast cell chymase and finally histamine in safranin-positive granules.