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. 2019 Mar 20;316(6):C767–C781. doi: 10.1152/ajpcell.00021.2019

Fig. 7.

Fig. 7.

Attenuation of cytochrome P450 1B1-deficient (Cyp1b1−/−) retinal astrocyte (AC) network formation in Matrigel and its restoration by reexpression of Cyp1b1. The ability of retinal ACs to undergo network formation on Matrigel was assessed by plating ACs on Matrigel as detailed in materials and methods. A: although Cyp1b1+/+ retinal ACs organized and formed a network on Matrigel, Cyp1b1−/− ACs failed to undergo network formation (×40). B: quantitative assessment of data. Mean number of branch points per five high-power fields (×100) was determined (****P < 0.0001; n = 4). C: reexpression of Cyp1b1 in Cyp1b1−/− retinal ACs using an adenovirus expression system. Western blot analysis of whole cell lysates from Cyp1b1−/− ACs infected with the adenovirus expressing empty vector (Vector) or mouse Cyp1b1 cDNA at different virus inputs (Av). β-Actin was used as a loading control. Please note lack of Cyp1b1 in vector control and increasing amounts of Cyp1b1 with increasing viral input. D: expression of Cyp1b1 restores the morphogenesis defect observed in Cyp1b1−/− ACs. Retinal ACs infected with adenovirus expressing empty vector or Cyp1b1 were plated in Matrigel. E: quantitative assessment of data as above. Please note significant restoration of morphogenesis in Cyp1b1−/− ACs expressing Cyp1b1 (Av-5 or 10 µl; *P < 0.05, ***P < 0.001, ****P < 0.0001; n = 3). Scale bars = 250 µm.