KLF13 promotes porcine adipocyte differentiation through PPARγ activation.

Background: Adipogenesis is tightly controlled by a complex network of transcription factors acting at different stages of differentiation. Kruppel-like factors (KLFs) as a family of zinc-finger transcription factors play diverse roles during cell differentiation and development in mammals. Results: In the present study, we showed that KLF13 acts as a key regulator regulating porcine adipocyte differentiation. The expression of KLF13 was markedly up-regulated during the early stage of porcine adipocyte differentiation, which was followed by expression of PPARγ. Porcine adipocyte differentiation was significantly attenuated by the addition of siRNA against KLF13, whereas overexpression of KLF13 resulted in enhanced porcine adipocyte differentiation. Using promoter deletion and mutation analysis, we identified a KLF13-binding site within -593/-577 region of the porcine PPARγ proximal promoter, indicating that KLF13 directly interacts with porcine PPARγ promoter. However, inhibition of KLF13 by siRNA did not impair mouse adipocyte differentiation. In addition, knockdown and/or overexpression of KLF13 in 3 T3-L1 cells all did not influence expression of PPARγ2. Conclusions: Collectively, our results suggest that KLF13 exist as a key pro-adipogenic transcription factor through transactivating PPARγ expression in porcine adipocyte differentiation, whereas no such effect was detected in mouse adipocyte differentiation. [ABSTRACT FROM AUTHOR]