Regulation of alpha 1-antichymotrypsin synthesis in cells of epithelial origin.
Oncostatin M, interleukin-1 and the glucocorticoid analog, dexamethasone, have been identified as potent stimulators of alpha 1-antichymotrypsin production in various cells of epithelial origin. Although being able to act individually, these factors exerted a dramatic increase in alpha 1-antichymotrypsin synthesis when administrated in combination. Their stimulatory effect was independent of the levels of constitutive synthesis of this inhibitor, which was already high in lung- and breast- and low in skin-derived epithelial cells. Since alpha 1-antichymotrypsin controls chymotrypsin-like proteinases which are released during inflammation, these data support the concept that local synthesis of this inhibitor may be important in reducing tissue damage associated with this process.
Cichy
J
J
Department of Microbiology and Immunology, Jagiellonian University, Kraków, Poland.
Potempa
J
J
Chawla
R K
RK
Travis
J
J
D003907:Dexamethasone / Q000494:pharmacology; D004848:Epithelium / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007375:Interleukin-1 / Q000494:pharmacology; D053683:Oncostatin M; D010455:Peptides / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D000514:alpha 1-Antichymotrypsin / Q000096:biosynthesis*
D007375:Interleukin-1; C508351:OSM protein, human; D010455:Peptides; D000514:alpha 1-Antichymotrypsin; D053683:Oncostatin M; D003907:Dexamethasone