C3H10T1/2多潜能干细胞成脂过程分为定向和分化两个阶段,骨形成蛋白4(BMP4)可以诱导其定向成前脂肪细胞.已有的研究表明,脂肪组织特异性敲除低密度脂蛋白受体相关蛋白1(Lrp1)的小鼠体重减轻,脂肪组织含量减少,揭示此基因对成脂具有重要作用.然而,目前尚不清楚Lrp1是否在成脂定向过程中发挥作用.采用小干扰RNA技术(RNAi),在体外水平研究低密度脂蛋白Lrp1对C3H10T1/2多潜能干细胞成脂定向的作用.分别在C3H10T1/2成脂的定向期和脂滴成熟期敲低Lrp1,通过显微镜下观察、油红O染色、Western blotting等实验证实,定向期而非脂滴成熟期敲低Lrp1显著抑制C3H10T1/2多潜能干细胞成脂.BMP4通过激活下游Smad1/5/8信号通路发挥作用,而敲低Lrp1显著抑制BMP4诱导的Smad1/5/8磷酸化.这些结果说明:敲低Lrp1通过下调Smad信号通路,抑制BMP4诱导的C3H10T1/2多潜能干细胞成脂定向. The process of adipogenic differentiation of C3H10T1 / 2 pluripotent stem cells is divided into two stages of orientation and differentiation, and BMP4 can induce its orientation into preadipocytes.Recent studies have shown that adipose tissue-specific knockdown of low density lipoprotein LRP1 mice showed reduced body weight and reduced adipose tissue content, suggesting that Lrp1 plays an important role in adipogenesis.However, it is not clear whether Lrp1 plays a role in adipogenesis.We used small interfering RNA (RNAi) was used to study the effect of low density lipoprotein (Lrp1) on the adipogenicity of C3H10T1 / 2 pluripotent stem cells in vitro.Lrp1 was knocked down in the directional and lipid droplet stages of C3H10T1 / 2 adipocytes and observed under a microscope , Oryzae O staining and Western blotting showed that Lrp1 knockdown significantly inhibited the adipogenic differentiation of C3H10T1 / 2 pluripotent stem cells in the targeted phase but not in the lipid droplet maturation stage.BMP4 played a role by activating the downstream Smad1 / 5/8 signaling pathway and knocking Low Lrp1 significantly inhibited BMP4-induced Smad1 / 5/8 phosphorylation.These results suggest that knockdown of Lrp1 inhibits BMP4-induced adipogenic targeting of C3H10T1 / 2 pluripotent stem cells by downregulating the Smad signaling pathway.