Department of Environmental Health, Boston University School of Public Health, Boston, MA, USA.
Department of Environmental Health, Boston University School of Public Health, Boston, MA, USA.
Toxicol In Vitro. 2020 Sep;67:104904. doi: 10.1016/j.tiv.2020.104904. Epub 2020 May 28.
3T3-L1 pre-adipocytes are used commonly to identify new adipogens, but this cell line has been shown to produce variable results. Here, potential adipogenic chemicals (identified in the ToxCast dataset using the Toxicological Priority Index) were tested for their ability to induce adipocyte differentiation in 3T3-L1 cells, OP9 cells and primary mouse bone marrow multipotent stromal cells (BM-MSC). Ten of the 36 potential adipogens stimulated lipid accumulation in at least one model (novel: fenthion, quinoxyfen, prallethrin, allethrin, pyrimethanil, tebuconzaole, 2,4,6-tris (tert-butyl)phenol; known: fentin, pioglitazone, 3,3',5,5'-tetrabromobisphenol A). Only prallethrin and pioglitazone enhanced lipid accumulation in all models. OP9 cells were significantly more sensitive to chemicals known to activate PPARγ through RXR than the other models. Coordinate effects on adipocyte and osteoblast differentiation were investigated further in BM-MSCs. Lipid accumulation was correlated with the ability to stimulate expression of the PPARγ target gene, Plin1. Induction of lipid accumulation also was associated with reduction in alkaline phosphatase activity. Allethrin, prallethrin, and quinoxyfen strongly suppressed osteogenic gene expression. BM-MSCs were useful in coordinately investigating pro-adipogenic and anti-osteogenic effects. Overall, the results show that additional models should be used in conjunction with 3T3-L1 cells to identify a broader spectrum of adipogens and their coordinate effects on osteogenesis.
3T3-L1 前脂肪细胞常用于鉴定新的脂肪生成细胞,但已证明该细胞系的结果存在差异。在这里,使用毒性优先指数(Toxicological Priority Index)从 ToxCast 数据集中鉴定出潜在的脂肪生成化学物质,测试它们在 3T3-L1 细胞、OP9 细胞和原代小鼠骨髓多能基质细胞(BM-MSC)中诱导脂肪细胞分化的能力。在至少一种模型中,有 10 种潜在的脂肪生成化学物质刺激脂质积累(新型:倍硫磷、喹氧酚、炔丙菊酯、丙烯菊酯、嘧啶苯胺、噻菌灵、2,4,6-三(叔丁基)苯酚;已知:芬替、吡格列酮、3,3',5,5'-四溴双酚 A)。只有炔丙菊酯和吡格列酮在所有模型中均增强了脂质积累。OP9 细胞对已知通过 RXR 激活 PPARγ的化学物质的敏感性明显高于其他模型。进一步在 BM-MSCs 中研究了对脂肪细胞和成骨细胞分化的协同作用。脂质积累与刺激 PPARγ 靶基因 Plin1 表达的能力相关。脂质积累的诱导也与碱性磷酸酶活性的降低相关。丙烯菊酯、炔丙菊酯和喹氧酚强烈抑制成骨基因表达。BM-MSCs 可用于协调研究促脂肪生成和抗成骨作用。总的来说,结果表明,应将其他模型与 3T3-L1 细胞结合使用,以鉴定更广泛的脂肪生成剂及其对成骨作用的协同作用。