title: Glycosylation-dependent cell adhesion molecule 1 (GlyCAM 1) is induced by prolactin and suppressed by progesterone in mammary epithelium.
abstract: Glycosylation-dependent cell adhesion molecule 1 (GlyCAM 1), a mucin-like endothelial glycoprotein, was induced by PRL and suppressed by progesterone in the mammary gland of mice, and in HC11 mouse mammary epithelial cells. Complementary DNA microarray analysis revealed that expression of GlyCAM 1 was reduced in the mammary gland of PRL-gene disrupted mice (PRL-/-) compared with control (PRL+/-) littermates. This result was confirmed by in situ hybridization and immunostaining. The messenger RNA (mRNA) encoding GlyCAM 1 was present in mammary epithelia of PRL-stimulated mice. Immunohistochemistry indicated that GlyCAM 1 protein was detectable both in mammary epithelia and in the ductal lumen in PRL+/- virgin mice, but not in PRL-/- mice. GlyCAM 1 mRNA was highly induced by grafting pituitary glands from normal littermates. Trace amounts of mRNA for GlyCAM 1 were detected by RT-PCR in mammary tissue of PRL-/- mice. Progesterone inhibited both basal and PRL-stimulated GlyCAM 1 transcription. In HC11 cells, GlyCAM 1 mRNA was induced in cells treated with insulin, dexamethasone, and PRL. Similar to the in vivo studies, progesterone inhibited the induction of GlyCAM 1 transcription. In CHO cells, PRL stimulated transcription of a luciferase reporter gene containing an 800-bp promoter fragment of GlyCAM 1, and progesterone partially suppressed the PRL effect. These data demonstrate that expression of GlyCAM 1 in mammary gland is under the control of both PRL and progesterone.
authors.affiliation: Department of Molecular and Cellular Physiology, University of Cincinnati, Ohio 45267, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Hou
authors.forename: J P
authors.initials: JP
authors.lastname: Bailey
authors.forename: A J
authors.initials: AJ
authors.lastname: Vomachka
authors.forename: M
authors.initials: M
authors.lastname: Matsuda
authors.forename: J A
authors.initials: JA
authors.lastname: Lockefeer
authors.forename: N D
authors.initials: ND
authors.lastname: Horseman
mesh_terms: D000818:Animals; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology; D004357:Drug Synergism; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007328:Insulin / Q000494:pharmacology; D008321:Mammary Glands, Animal / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism*; D051379:Mice; D009077:Mucins / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D011374:Progesterone / Q000494:pharmacology*; D011388:Prolactin / Q000172:deficiency / Q000235:genetics / Q000494:pharmacology*; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D005938:Glucocorticoids; D007328:Insulin; D009077:Mucins; D012333:RNA, Messenger; C075185:sulfated glycoprotein p50; D011374:Progesterone; D003907:Dexamethasone; D011388:Prolactin