Fig 1: HIF-1α mRNA expression in extrahepatic organs of the BDL model. Heat maps of HIF-1α and inducers and inhibitors of HIF-1α in transcriptome analysis of extrahepatic organs (control vs. CLD and CLD vs. ACLF) (A), mRNA expression levels of HIF-1α (B), inducers of HIF-1a (C) and inhibitors (D) in specimens from small bowel. Respective mRNA expression levels in specimens from skeletal muscle tissue (E–G). * p < 0.05, ** p < 0.01.
Fig 2: HIF-1α expression in liver tissue. mRNA expression levels of HIF-1α (A), inducers of HIF-1α (B) and inhibitors (C) in the cholestatic model (BDL) causing chronic liver disease (CLD, n = 5); acute-on-chronic liver failure was induced by intravenous lipopolysaccharide injection (n = 4). Respective mRNA expression levels in the CCl4 model causing CLD (n = 8 with CLD, n = 14 with ACLF) (D–F). Increased HIF-1α protein expression was confirmed by Western blotting, and signs of NFκB1 pathway activation were reflected by increased expression of IκB and pIκB (G). Effects on mRNA expression levels of downstream genes of HIF are depicted in (H). Note: (G) For the detection of HIF-1α expression via Western blotting, 30 ng of recombinant Human HIF-1 alpha protein (#ab154478, Abcam, Cambridge, MA, USA) as a positive control (pos+), 50 µg of HeLa whole-cell extract as a negative control (neg−) and 100 µg of whole-protein extract from mouse liver tissues (CTRL, CLD and ACLF, respectively) were analyzed. For IκB and pIκB detection, 50 µg of HEK293T cell extract was used (positive control for IκB and pIκB) instead of HeLa extract, and only 50 µg of whole-protein extract from mouse liver tissues was used (CTRL, CLD, ACLF). * p < 0.05, ** p < 0.01, *** p < 0.001.
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