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. Author manuscript; available in PMC: 2024 Dec 13.
Published in final edited form as: Cell Rep. 2024 Sep 25;43(10):114789. doi: 10.1016/j.celrep.2024.114789

Figure 5. Placental Sod3 KO inhibits the FGF-prolactin axis in the pituitary gland.

Figure 5.

(A) Reactome pathway analysis of placental Sod3f/f and Sod3−/− dams.

(B) Prl mRNA expression levels of 100 ng/mL recombinant fibroblast growth factor (FGF)1-, FGF2-, or FGF4-stimulated mouse primary pituitary cells with or without 10 μM FGF receptor (FGFR) inhibitors. BGJ398: FGFR1/2/3 inhibitor, PD16686: FGFR1 inhibitor, H3B-6527: FGFR4 inhibitor.

N = 5; three technical replicates for each group; **p < 0.01 vs. FGF1-control, ††p < 0.01 vs. FGF2-control, and ‡‡p < 0.01 vs. FGF4-control.

(C) Prl mRNA expression levels in recombinant FGF1-, FGF2-, or FGF4-stimulated primary pituitary cells from placental Sod3f/f and Sod3−/− dams on day 10 after delivery.

(D) Phosphorylation levels of FGFR-induced signaling molecules in recombinant FGF1-, FGF2-, or FGF4-stimulated primary pituitary cells from placental Sod3f/f and Sod3−/− dams.

N = 3 in each group; three biological and technical replicates for each group.