KLF2 may suppress chicken adipogenesis by enhancing the GATA2 transcription

Kruppel-like factor 2 (KLF2) acts as an essential modulator of adipogenesis; nevertheless, the exact molecular pathways governing its role remain uncharacterized. This investigation characterized the expression profile of KLF2 in human adipose tissue and elucidated the mechanisms by which KLF2 modulates adipogenesis in avian models. The KLF2 mRNA expression in human adipose tissues was substantial and exhibited significant heterogeneity influenced by gender and anatomical location, suggesting that KLF2 regulated adipose tissue functionality. In chicken preadipocytes ICP1, the KLF2 protein increased at the first 24 h of oleate-induced adipogenic differentiation and subsequently decreased over time. KLF2 facilitated the cellular proliferation of ICP1 cells (P<0.05). Moreover, KLF2 overexpression inhibited differentiation of chicken preadipocytes ICP1 (P<0.05). KLF2 also increased the density of mitochondria and mitochondrial cristae in ICP1 cells. RNA seq and luciferase reporter assays demonstrated that KLF2 suppressed the expression of genes in PPAR signaling pathway in ICP1 cells. Additionally, KLF2 interacted with the promoter region of chicken GATA2 and upregulated GATA2 transcription in ICP1 cells. In summary, KLF2 potentially influences the PPAR signaling cascade, mitochondrial bioenergetics, and GATA2 gene expression to enhance the proliferation of avian preadipocytes while inhibiting their differentiation. The ICP1 cells were inoculated into 6-well plates, and when the cells reached 60%-80% confluence, the given plasmids of pCMV-myc or pCMV-myc-KLF2 were transfected into the cells using ExFect® Transfection Reagent (#T101-02, Vazyme, Nanjing, China).After the transfection for 48 h, the ICP1 cells were harvested using TRIzol™ Reagent (#15596026, Invitrogen, Carlsbad, CA) for subsequent RNA sequencing.