title: Opposite effects of transforming growth factor alpha and epidermal growth factor on mouse placental lactogen I secretion.
abstract: This study was undertaken to determine whether transforming growth factor alpha (TGF-alpha) regulates the production of mouse placental lactogen I (mPL-I) and mPL-II in a manner that is similar to that of epidermal growth factor (EGF), which was previously shown to stimulate mPL-I secretion and inhibit mPL-II secretion. In contrast to the activity of EGF, human (h) and rat (r) TGF-alpha (each at 100 ng/ml) inhibited secretion of mPL-I by placental cells isolated from mice on day 7 of pregnancy. Maximum inhibition of mPL-I secretion occurred on the third day of a 5-day culture period and ranged between 37% and 56% in multiple trials. Incubation of cells with hTGF-alpha and EGF was not followed by a change in the mPL-I concentration of the medium, suggesting the peptides antagonized each other's effects. hTGF-alpha and rTGF-alpha inhibited secretion of mPL-II; maximum inhibition ranged between 62% and 84% in multiple trials. The lowest concentrations of hTGF-alpha that affected mPL-I and mPL-II secretion were 10 ng/ml and 1 ng/ml, respectively. EGF and hTGF-alpha bound to the same receptors on placental cells, as assessed by cross-linking, and both peptides stimulated receptor phosphorylation, as assessed by Western blot analysis. There are three types of mPL-containing cells in placental cultures: cells that contain only mPL-I, cells that contain only mPL-II, and cells that contain both mPLs. The percentage of each type of mPL-containing cell in the culture was determined by immunostaining. hTGF-alpha affected the differentiation of the subpopulations of PL-containing cells in a manner that differed from that of EGF. The data suggest that TGF-alpha and EGF do not regulate the production of mPL-I and mPL-II in a similar manner.
authors.affiliation: Department of Biology, University of California, Santa Cruz 95064, USA.
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: L
authors.initials: L
authors.lastname: Ogren
authors.forename: H
authors.initials: H
authors.lastname: Kurachi
authors.forename: K
authors.initials: K
authors.lastname: Hirota
authors.forename: T
authors.initials: T
authors.lastname: Imai
authors.forename: F
authors.initials: F
authors.lastname: Talamantes
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D004815:Epidermal Growth Factor / Q000378:metabolism / Q000494:pharmacology*; D066246:ErbB Receptors / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007700:Kinetics; D051379:Mice; D019000:Phosphotyrosine; D010920:Placenta / Q000187:drug effects / Q000502:physiology*; D010928:Placental Lactogen / Q000032:analysis / Q000096:biosynthesis* / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D011994:Recombinant Proteins / Q000032:analysis; D016211:Transforming Growth Factor alpha / Q000378:metabolism / Q000494:pharmacology*; D014443:Tyrosine / Q000031:analogs & derivatives / Q000032:analysis
chemical_list: D011994:Recombinant Proteins; D016211:Transforming Growth Factor alpha; C062303:placental lactogen II; C085699:placental lactogen I, rat; D019000:Phosphotyrosine; D014443:Tyrosine; D004815:Epidermal Growth Factor; D010928:Placental Lactogen; D066246:ErbB Receptors