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On mast cell‐mediated mitogenesis in normal and hyperplastic mesenterial windows in female rats
Author(s) -
BERGSTRÖM STEFAN,
SIMONSEN MAGNUS,
NORRBY KLAS
Publication year - 1989
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1989.tb00487.x
Subject(s) - mast cell , hyperplasia , endocrinology , medicine , biology , histamine , connective tissue , cell , pathology , immunology , genetics
The outcome of the mast cell‐mediated mitogenesis in hyperplastic membranous mesenterial windows of lactating rats as well as in normal mesenterial windows of age‐matched and young virgin female rats was studied quantitatively in vivo and in organ culture. Besides elucidating the effect of age and tissue hyperplasia on mitogenic reponsiveness, this approach should provide some insight into the pathogenic mechanics of the previously reported supranormal mast cell‐mediated mitogenic reaction that emerges in similarly hyperplastic mesenterial windows of diabetic rats. Mast cell secretion was elicited by Compound 48/80 and the histamine release, which was quantified fluorometrically, was unaffected by lactation. The young female rats showed a statistically significant mast cell‐dependent mitogenesis taken as the mitotic index and the fraction of the predominating fibroblasts and mesothelial cells in the (S+G2) cell cycle phases after Feulgen‐DNA absorption analysis of the cells in situ. Although there was an age‐dependent decrease in mitogenesis, the older lactating and non‐lactating virgin control rats also showed mast cell‐mediated mitogenesis measured as the specific DNA activity. The hyperplastic mesenterial tissue of the lactating animals showed a virtually normal mitogenic reactivity following local mast cell secretion, but at a lower level than in the age‐matched controls. This finding suggests that the supranormal mast cell‐mediated mitogenesis previously found in the hyperplastic mesenterial windows of diabetic animals is causally related to the diabetic condition rather than to the hyperplastic state of the test tissue.