Department of Functional Morphology, Graduate School of Pharmaceutical Sciences, Niigata University of Pharmacy and Medical and Life Sciences, Niigata, 956-8603, Japan.
Department of Functional Morphology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Medical and Life Sciences, 265-1 Higashijima, Akiha-ku, Niigata, 956-8603, Japan.
Sci Rep. 2024 Aug 29;14(1):20049. doi: 10.1038/s41598-024-70930-5.
Adipogenesis involves intricate molecular mechanisms regulated by various transcription factors and signaling pathways. In this study, we aimed to identify factors specifically induced during adipogenesis in the human preadipocyte cell line, SGBS, but not in the mouse preadipocyte cell line, 3T3-L1. Microarray analysis revealed distinct gene expression profiles, with 1460 genes induced in SGBS cells and 1297 genes induced in 3T3-L1 cells during adipogenesis, with only 297 genes commonly induced. Among the genes uniquely induced in SGBS cells, we focused on GALNT15, which encodes polypeptide N-acetylgalactosaminyltransferase-15. Its expression increased transiently during adipogenesis in SGBS cells but remained low in 3T3-L1 cells. Overexpression of GALNT15 increased mRNA levels of CCAAT-enhancer binding protein (C/EBPα) and leptin but had no significant impact on adipogenesis in SGBS cells. Conversely, knockdown of GALNT15 suppressed mRNA expression of adipocyte marker genes, reduced lipid accumulation, and decreased the percentage of cells with oil droplets. The induction of C/EBPα and peroxisome proliferator-activated receptor γ during adipogenesis was promoted or suppressed in SGBS cells subjected to overexpression or knockdown of GALNT15, respectively. These data suggest that polypeptide N-acetylgalactosaminyltransferase-15 is a novel regulatory molecule that enhances adipogenesis in SGBS cells.
脂肪生成涉及各种转录因子和信号通路调节的复杂分子机制。在这项研究中，我们旨在鉴定在人类前体脂肪细胞系 SGBS 中脂肪生成过程中特异性诱导的因子，而不在小鼠前体脂肪细胞系 3T3-L1 中诱导。微阵列分析显示出明显不同的基因表达谱，在 SGBS 细胞中诱导了 1460 个基因，在 3T3-L1 细胞中诱导了 1297 个基因，只有 297 个基因共同诱导。在 SGBS 细胞中特异性诱导的基因中，我们重点关注编码多肽 N-乙酰半乳糖胺基转移酶 15（GALNT15）的基因。其表达在 SGBS 细胞的脂肪生成过程中短暂增加，但在 3T3-L1 细胞中保持较低水平。GALNT15 的过表达增加了 CCAAT 增强子结合蛋白（C/EBPα）和瘦素的 mRNA 水平，但对 SGBS 细胞的脂肪生成没有显著影响。相反，GALNT15 的敲低抑制了脂肪细胞标记基因的 mRNA 表达，减少了脂质积累，并降低了具有油滴的细胞百分比。在 SGBS 细胞中，过表达或敲低 GALNT15 分别促进或抑制 C/EBPα 和过氧化物酶体增殖物激活受体 γ 在脂肪生成过程中的诱导。这些数据表明，多肽 N-乙酰半乳糖胺基转移酶 15 是一种增强 SGBS 细胞脂肪生成的新型调节分子。
