Fig. 7. The effects of deletion of HIF1 are mammary epithelial cell autonomous. Primary Hif1a^f+/f+ mammary epithelial cells were infected with either Adeno-ßgal or Adeno-Cre and transplanted into the cleared fat pads of female host mice in order to generate wild-type (A) and Hif1a^–/– (B) epithelial outgrowths, respectively. Paraffin wax-embedded sections harvested from mice on the date of birth (without prior weaning of pups) were stained with Mason's Trichrome. Scale bar: 50 µm (n=3 mice with 100% outgrowths/genotype). Outgrowths derived from Hif1a^–/– mammary epithelial cells recapitulated the phenotype observed in intact Hif1a^–/– glands. Note the lack of milk products (indicated by yellow stars) in the Hif1a^–/– outgrowth, and the presence of large, trapped lipid droplets within the epithelial cells (B, right white arrow). In addition, there was an abnormal thickening of collagen fibers (stained blue; B, left white arrow) around the alveoli in these outgrowths compared with wild type (black arrow). (C,D) Glut1 (brown staining) was detected in paraffin wax-embedded sections prepared from transplanted outgrowths. Compared to wild type (C), expression of Glut1 in the Hif1a null outgrowths (D) was less intense and more patchy.

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