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. Author manuscript; available in PMC: 2019 Jul 15.
Published in final edited form as: Cancer Res. 2018 Jun 29;78(14):3877–3887. doi: 10.1158/0008-5472.CAN-17-2892

Figure 3.

Figure 3

Complementary studies with CypA+/+ and −/− mammary gland cross-transplants and pharmacologic inhibition of CypA with NIM811 reveal that the defect in mammary gland development CypA−/− mice is epithelial and is also noted when CypA is inhibited following initial mammary development. (a) Cross-transplant of CypA+/+ and −/− mammary epithelium and stroma reveals that the defect in mammary alveolar budding in CypA−/− mice is epithelial. Following mammary ductal clearance at three weeks of age, epithelial cross-transplants were performed from mice aged 5-10 weeks of age. Analysis of the resultant mammary tree occurred by whole mount analysis when the recipient mice were 14 weeks of age. Bar = 750 microns. (b) Pharmacologic inhibition of CypA with NIM811 results in defective alveolar budding as seen in the mammary glands of CypA−/− mice. Nu−/− mice were treated with the CypA inhibitor, NIM811 (an analog of cyclosporine A). Mammary glands from virgin mice were harvested at week 14 after 6 weeks of treatment with NIM811 (100 ug/kg/day po) or control carrier and processed for whole mount. (Bar = 1.5mm).