Skip to main content
. 2011 May;163(2):299–312. doi: 10.1111/j.1476-5381.2011.01208.x

Figure 3.

Figure 3

Doxorubicin (DOX) does not inhibit HIF expression and transactivation capacity. (A) Immunoblot analysis of nuclear extracts of untreated H9c2 cells (C) and cells exposed for 24 h to doxorubicin, for 3 h to dexrazoxane (DRZ) alone or pretreated with DRZ for 3 h and then exposed to DOX, using the anti-HIF-1α antibody. The blots were reprobed using the antibody against TFIID as a loading control. The panel shows one representative blot and the densitometric quantification relative to C-values. (B) Relative luciferase activity (RLA) in H9c2 cells transiently transfected with a construct in which luciferase was controlled by an HRE multimer and treated as described for panel A. The cells were cotransfected using a control vector containing the Renilla luciferase gene. Luciferase activity was determined after 24 h, corrected for transfection efficiency on the basis of Renilla luciferase activity and normalized to the activity recorded in untreated cells (arbitrarily set to 1). Mean values ± SD. *P < 0.001; ***P < 0.01; #P < 0.05, n = 3. HIF, hypoxia-inducible factor; TFIID, transcription factor II D.