Crucial role of estrogen for the mammalian female in regulating semen coagulation and liquefaction in vivo
Fig 1
Loss of ESR1 in uterine epithelial cells leads to a semen liquefaction defect in female mice.
A. Immunohistochemical analysis indicates the expression of ESR1 in the uteri of Esr1f/f mice and its absence in Wnt7aCre/+;Esr1f/f animals at 0.5 dpc. LE = luminal epithelial cells; GE = glandular epithelial cells. B. Gross morphology of the reproductive tract of Esr1f/f and Wnt7aCre/+;Esr1f/f animals at 0.5 dpc. C. Diameters of the uteri prior to dissection at 0.5 dpc, n = 9–10 mice/genotype. D. Total fluid volume (μL) collected from the uteri of Esr1f/f and Wnt7aCre/+;Esr1f/f animals at 0.5 dpc, n = 3 mice/genotype. E. Expression of Aqp transcripts in the uteri at 0.5 dpc, n = 4–5 mice/genotype. F. Liquefaction time measured as the time it took for semen collected from the uteri at 0.5 dpc to fill a 25-μL capillary tube (minutes). Note that the liquefaction time for semen collected from Wnt7aCre/+;Esr1f/f uteri was over 1 h (>60 min), n = 3 mice/genotype. G. Hematoxylin & Eosin (H&E) staining of uterine samples collected at 0.5 dpc, n = 9–10 mice/genotype. H. Sperm density was determined from the semen within the uterine lumen per microscopic field of H&E stained images and normalized to mm2, n = 7–10 mice/genotype. I. Total sperm number in the uterus was calculated after normalization to the total fluid volume collected, n = 3 mice/genotype. J. Percentage of sperm motility per microscopic field in the semen collected from the uteri of Esr1f/f and Wnt7aCre/+;Esr1f/f animals at 0.5 dpc, n = 3 mice/genotype. *, #p<0.05; significant difference between Esr1f/f and Wnt7aCre/+;Esr1f/f animals, unpaired t-test or two-way ANOVA, respectively. Representative images are shown. Graphs represent mean±SEM.