Fig. 5.

Muc1 transactivates gene targets of HIF-1: lactate dehydrogenase A (LDHA) and enolase (ENO). Kidneys of Muc1 KO mice and congenic control C57BL/6 mice were subjected to IRI for 19 min and recovery for 0–72 h. Products of HIF-1 gene targets were measured by immunoblot analysis of 60 μg kidney homogenates for LDHA (A and C) and ENO (B and D) and then β-actin as a loading control (E). Bands on immunoblots were quantified and presented as means ± SE relative to that of control mice at t = 0 (set as 1). Profiles of LDHA and ENO for Muc1 KO and control mouse kidneys were significantly different by two-way ANOVA (P < 0.01 and P < 0.05, respectively, as indicated). Levels of LDHA were significantly increased in control mice at 24 h (**P < 0.01) and 72 h (*P < 0.05) of recovery compared with 0 h. Levels of LDHA at 4, 24, and 72 h of recovery were significantly different between Muc1 KO and control mice (P < 0.05). Levels of ENO were significantly increased in control mice at 24 h (*P < 0.05). Levels of ENO at 24 h were significantly different between Muc1 KO and control mice (P < 0.05).