title: Interleukin-1 receptor-ligand interactions modulate interstitial collagenase-1 production by human endometrial fibroblasts.
abstract: The expression of interstitial collagenase-1 in the cycling human endometrium is restricted to the perimenstrual phase and is a key event for matrix degradation that initiates menstruation. In the absence of ovarian steroids, collagenase production by endometrial fibroblasts is induced by epithelial cell-derived interleukin-1alpha. Media conditioned by endometrial epithelial cells were found to contain interleukin-1alpha but not interleukin-1beta, and their capacity to induce collagenase production by endometrial fibroblasts correlated with interleukin-1alpha concentration in a saturable manner. Collagenase induction by recombinant interleukin-1alpha was severely inhibited by interleukin-1 receptor antagonist alone and abolished by its combination with soluble interleukin-1 type-II receptor. By contrast, the association of the receptor antagonist with soluble type-I receptor was less effective than each factor alone. Induction of collagenase by epithelial cell-conditioned media was severely inhibited by neutralizing interleukin-1alpha antibodies, whereas the combination of receptor antagonist with soluble type-II receptor proved less effective. We conclude that the collagenase response of endometrial fibroblasts to epithelial cell-derived interleukin-1alpha is effectively blocked in vitro by soluble members of the interleukin-1 family and can thus be modulated in vivo by these or other local factors.
authors.affiliation: Cell Biology Unit, Christian de Duve Institute of Cellular Pathology, Brussels, Belgium.
authors.forename: C F
authors.initials: CF
authors.lastname: Singer
authors.forename: E
authors.initials: E
authors.lastname: Marbaix
authors.forename: P
authors.initials: P
authors.lastname: Lemoine
authors.forename: Y
authors.initials: Y
authors.lastname: Eeckhout
authors.forename: P J
authors.initials: PJ
authors.lastname: Courtoy
mesh_terms: D002478:Cells, Cultured; D017364:Collagenases / Q000096:biosynthesis*; D017077:Culture Media, Conditioned / Q000494:pharmacology; D004717:Endometrium / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism; D005260:Female; D005347:Fibroblasts / Q000187:drug effects / Q000201:enzymology*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000494:pharmacology; D020781:Matrix Metalloproteinase 1; D017472:Receptors, Interleukin-1 / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D012795:Sialoglycoproteins / Q000494:pharmacology; D012995:Solubility
chemical_list: D017077:Culture Media, Conditioned; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D011994:Recombinant Proteins; D012795:Sialoglycoproteins; D017364:Collagenases; D020781:Matrix Metalloproteinase 1