Abstract
The present study aimed to investigate the transcriptional regulation of Kbtbd11 in adipose tissue. To elucidate the physiological role of Kbtbd11 gene expression, adipose Kbtbd11 mRNA expression levels were estimated under various feeding states in wild-type mice. Kbtbd11 expression increased in a time-dependent manner in the adipose tissue in mice fed on chow diet, whereas the promotion of Kbtbd11 mRNA expression by refeeding was attenuated in mice fed on high-fat (HF) diet, suggesting the suppression of Kbtbd11 mRNA expression under HF diets and that changes in mRNA levels were associated with regulation of the transcription activity of Kbtbd11 by some transcription factors. To investigate the transcriptional regulation of Kbtbd11, the fragment upstream of either mouse Kbtbd11 or human KBTBD11 promoter was inserted into a luciferase vector. Luciferase reporter assays revealed that both mouse and human KBTBD11 promoter activity was increased by USF1. Direct USF1 binding to the Ebox in the Kbtbd11 promoter was confirmed by electrophoretic mobility shift and chromatin immunoprecipitation assays. In addition, the adipocyte differentiation marker levels increased instantly in Kbtbd11-overexpressing Usf1 knockdown cells than in Usf1 knockdown cells. These results imply an association of between Kbtbd11 with Usf1 expression and suggest the involvement of Kbtbd11 in a novel adipogenesis pathway.
Highlights
Kelch repeat and BTB domain-containing 11 (KBTBD11) is a member of the KBTBD subfamily, which comprised BTB/POZ and Kelch domains
We have previously reported that Kbtbd11 is involved in nutritional regulation and is highly expressed in the epididymal white adipose tissue in diet-induced obesity (DIO) mice compared with that in mice fed on chow diet [2]
We have previously reported that Kbtbd11 mRNA expression increases in a time-dependent manner during 3T3-L1 differentiation and increases significantly in epididymal white adipose tissue (eWAT) under feeding status and obesity [2]
Summary
Kelch repeat and BTB domain-containing 11 (KBTBD11) is a member of the KBTBD subfamily, which comprised BTB/POZ and Kelch domains. KBTBD11 expression is significantly decreased in tumor tissues compared with adjacent paired normal tissues [4]. Kbtbd11-overexpressing 3T3-L1 promotes MCE, which leads to the expression of adipocyte differentiation markers—C/ebpa and Pparg, and induces lipid accumulation [2], suggesting that Kbtbd expression levels play a major role in MCE and influence triglyceride accumulation and adipocyte differentiation. In this context, the present study aimed to clarify the transcriptional regulation of Kbtbd to elucidate the functions underlying the role of Kbtbd in adipocyte differentiation
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