Two cell types isolated and purified to homogeneity from human decidua obtained at 8-17 weeks of gestation were shown immunocytochemically to correspond to decidual and epithelial cells in the tissue of origin. The decidual cells reacted with antihuman PRL antiserum, and epithelial cells reacted with antiserum against keratin, an epithelial cell marker. Decidual and epithelial cells were cultured separately to determine their abilities to release PRL to the medium. Decidual cells released 140-410 ng PRL/mg protein in 24 h, whereas no PRL was detectable in cultures of isolated epithelial cells. These homogeneous preparations provide an excellent system with which to study the regulation of PRL production and other biochemical properties of decidual components.

No abstract

The lung of adult man contains several times more 5'-nucleotidase (EC 3.1.3.5), alkaline phosphatase (EC 3.1.3.1) and γ-glutamyl-transpeptidase (EC 2.3.2.2) per gram than does that of the 12- to 16-week fetus. In rat lung, too, there is a drastic developmental rise in these activities. Opposite changes in two of the enzymes occur during hepatic differentiation: alkaline phosphatase decreases in the rat, and γ-glutamyl-transpeptidase is ten times higher in the fetal than in the adult liver of both species.

Protein kinase C(PKC) activity and DNA synthesis were measured in human fetal bone marrow fibroblasts following treatment with tumor necrosis factor alpha (TNFα)(500 U/ml) or conditioned media containing natural cell proliferation inhibitor (CM‐NCPI). Treatment with TNFα led to growth stimulation (120 ± 7% of control in 24 h, 141 ± 6% in 72 h). At the same time particulate PKC activity diminished, reaching 55 ± 8% of control in 24 h and remaining at this level at 72 h. CM‐NCPI treatment of the cells resulted in a decrease in DNA synthesis (by 39 ± 6% in 2 h, by 58 ± 5% in 24 h, and by 78 ± 8% in 72 h). This was accompanied by a significant rise in particulate PKC activity which increased over 3‐fold in 2 h, over 5‐fold in 24 h, and up to 11‐fold in 72 h. This 11‐fold elevation was maintained after 2 week exposure of the fibroblasts to CM‐NCPI. The PKC inhibitor neomycin abolished CM‐NCPI induced growth inhibition, whereas PKC activator 12‐O‐tetradecanoylphorbol 13‐acetate intensified it. These results suggest that CM‐NCPI acts as PKC activator and that negative growth regulation by extracellular agents may involve stimulation of PKC activity.

No abstract