Fig. 2.

Effect of estrogen on mammary ductal growth in the absence of leptin-dependent STAT3 signaling. A, Female mice lacking leptin-dependent STAT3 signaling (s/s) or their WT counterparts were treated with either corn oil (Oil) or 0.03 μg of 17β-estradiol-valerate (E, n = 3–4 mice for each genotype × estrogen combination). Injections were initiated at 21–23 d of age and were given every 3 d for 4 consecutive weeks. A second group of WT mice were ovariectomized at 22–26 d of age and treated similarly with oil or E (OVX WT, n = 2 per group). The right abdominal mammary gland was analyzed by whole-mount staining. B, Uterine tissue weights were measured at the end of the treatment period. The significant effect of estrogen (E) treatment is shown. Each bar represents the mean ± se of three to four mice. C, Serum was collected from WT and s/s mice at 4 and 6 wk of age and assayed for estrogen concentrations by RIA. Each bar represents the mean ± se of eight mice. D, Mammary tissues containing EPI were collected from female mice lacking leptin-dependent STAT3 signaling (s/s) or their WT counterparts at 4 wk of age. Total RNA was analyzed by real-time PCR for the mRNA abundance of ERα, PR, and amphiregulin. Each bar represents the mean ± se of eight mice.