Figure 3
FFA and lactate potentiate HIF1α protein activity in mouse chondrocytes.
(a) Immunoblotting assay of HIF1α in mouse primary chondrocytes treated with normal oxygen (Normoxia, 20% O2), low oxygen (hypoxia, 0.1% O2), BSA (5%), FFA (200 μM), lactate (25 mM) and vehicle control for 24 h. (b~d) Protein stability of HIF1α in response to the treatment with hypoxia. (b), 200 μM FFA (c) and 25 mM lactate (d) for 24 h (n = 4, **P < 0.01). (e) Protein stability of HIF1α in response to the treatment with full or fractionated (>3 KD or <3 KD) serum from the 8-week ND or HFD-feeding mice. (n = 3, **P < 0.01). (f~h) Transcriptional activity of VEGF promoter in response to the treatment with hypoxia (f), 200 μM FFA (g) and 25 mM lactate (h) for 24 h (n = 3, *P < 0.05 and **P < 0.01). (i) Transcriptional activity of VEGF promoter in response to the treatment with full or fractionated (>3 KD or <3 KD) serum from the 8-week ND or HFD-feeding mice. (n = 3, **P < 0.01). Relative luc. activity: relative luciferase activity.
