Department of Oral Physiology, BK21 PLUS Project, School of Dentistry, Pusan National University, Yangsan 50610, Korea.
Department of Dental Pharmacology, BK21 PLUS Project, School of Dentistry, Pusan National University, Yangsan 50610, Korea.
Int J Mol Sci. 2018 Dec 10;19(12):3971. doi: 10.3390/ijms19123971.
Gastrin-releasing peptide (GRP), a member of bombesin-like peptides, and its receptor (GRP-R) play an important role in various physiological and pathological conditions. In this work, we investigated the role of GRP-R on adipogenesis in 3T3-L1 adipocytes. The expression of GRP-R was significantly increased during the adipocyte differentiation of 3T3-L1 cells. The inhibition of GRP-R by the antagonist RC-3095 affected adipogenesis in 3T3-L1 cells, which reduced lipid accumulation and regulated the expression of adipogenic genes. Moreover, cyclic AMP response element-binding protein (CREB) directly bound to the GRP-R promoter upon exposure to adipogenic stimuli. The down-regulation of GRP-R by the knockdown of CREB inhibited adipocyte differentiation of 3T3-L1 cells. Together these results suggest that the regulation of GRP-R activity or expression has an influence on adipogenesis through regulating adipogenic related genes.
胃泌素释放肽(GRP)是脑肠肽家族的一员,其受体(GRP-R)在多种生理和病理条件中发挥重要作用。在这项工作中,我们研究了 GRP-R 在 3T3-L1 脂肪细胞成脂分化中的作用。在 3T3-L1 细胞的脂肪细胞分化过程中,GRP-R 的表达显著增加。GRP-R 的拮抗剂 RC-3095 的抑制作用影响 3T3-L1 细胞的成脂分化,减少脂质积累并调节脂肪生成基因的表达。此外,环磷酸腺苷反应元件结合蛋白(CREB)在受到成脂刺激时直接与 GRP-R 启动子结合。通过 CREB 的敲低下调 GRP-R 抑制 3T3-L1 细胞的脂肪细胞分化。这些结果表明,通过调节脂肪生成相关基因,GRP-R 活性或表达的调节对脂肪生成有影响。