FIG. 3.
In vivo transgene expression is upregulated by the HSV1 TK gene sequence carried in HCAd vectors, but not in Ad vectors. Five mice per group were stereotactically injected with 1.0 × 106 vgs of each of the high-capacity adenoviral vectors HCAd-mCMV.βgal, HCAd-mCMV.βgal.TK, and HCAd-mCMV.βgal.WPRE and with Ad-mCMV.βgal, Ad-mCMV.βgal.TK, and Ad-mCMV.βgal.WPRE. (a) Low-power microphotographs showing β-Gal immunoreactivity in representative striatal sections from mice injected intracranially with the different vectors; (b) Numbers of β-Gal-expressing cells per brain. The β-Gal staining was performed 5 days after injection, when animals were perfusion fixed, and transgene expression was determined by immunocytochemistry. The data are expressed as β-Gal-expressing cells per mouse striatum. β-Gal-expressing cells were quantified utilizing Stereo Investigator software, version 5.00 (Microbrightfield, Inc., Colchester, VT). (c) Five mice per group were stereotactically injected with 1.0 × 106 vgs of each of the high-capacity adenoviral vectors HCAd-mCMV.βgal, HCAd-mCMV.βgal.TK, and HCAd-mCMV.βgal.WPRE and with Ad-mCMV.βgal, Ad-mCMV.βgal.TK, and Ad-mCMV.βgal.WPRE. The enzymatic activity (β-Gal activity in brain lysates) was measured 3 days after intracranial injection of vectors, following animal perfusion with oxygenated Tyrode's solution. After testing for normality, all data were analyzed by one-way ANOVA followed by the Tukey-Kramer multiple comparison test. *, P < 0.05 versus control group, injected with a β-Gal-encoding vector.