Figure 4.

HIF-1α promotes the accumulation of LDs through SCD1. (A) The volcano map of gene changes in fibroblasts (NIH 3T3-HIF-1α-MOCK and NIH 3T3-HIF-1α-KO) by RNA-sequencing. (B and C) Signature genes involved in lipid metabolism were listed and validated by RT-PCR in fibroblasts (NIH 3T3-HIF-1α-MOCK and NIH 3T3-HIF-1α-KO) (N = 3). (D and E) The RNA and protein levels of SCD1 in fibroblasts (NIH 3T3) that were treated with hypoxia (1% O₂), TGF-β1 and LLC-CM. (F) The protein expression of SCD1 in fibroblasts (NIH 3T3-HIF-1α-MOCK and NIH 3T3-HIF-1α-KO cells) transfected with the SCD1-overexpression plasmid. (G) The relative promoter activity of mSCD1 in NIH 3T3-MOCK and NIH 3T3-KO cells. (H) The expression of bound proteins of HIF-1α in 5'-biotin labeled probes corresponding to the S85 fragment of mSCD1 promoter or a nonspecific probe (NSP) that was incubated with NIH 3T3 cell lysates and streptavidin beads. (I and J) The relative expressions of the RNA and protein of SCD1 were determined in the SCD1-MOCK and SCD1-OVER cells (NIH 3T3) (N = 3). (K) The BODIPY staining of the LDs in the SCD1-MOCK cells and SCD1-OVER cells (NIH 3T3). Data are shown as the Mean±SD; *p < 0.05, **p < 0.01, ***p < 0.001.