G protein-coupled estrogen receptor 1 mediates proliferation and adipogenic differentiation of goat adipose-derived stem cells through ERK1/2-NF-κB signaling pathway.
G protein-coupled estrogen receptor 1 mediates proliferation and adipogenic differentiation of goat adipose-derived stem cells through ERK1/2-NF-κB signaling pathway.
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DOI：
10.3724/abbs.2022031
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发表时间：
2022-04-25
影响因子：
3.7
通讯作者：
Ma B
中科院分区：
文献类型：
--
作者：
Zhao Y;Liu C;Gao Z;Shao D;Zhao X;Wei Q;Ma B
脂肪组织的形成和适度的脂肪沉积对于畜肉的生产性能和食用品质非常重要。脂肪干细胞的自我更新和成脂分化负责脂肪组织的形成和发育。此外，据报道，靶向 G 蛋白偶联雌激素受体 1 (GPER1) 的雌激素可调节组织和器官发育过程中的细胞增殖和分化。然而，山羊脂肪干细胞 (gADSC) 中雌激素、GPER1、增殖和成脂分化之间的潜在相关性仍不清楚。在此，我们证明 17β-雌二醇可增强 gADSC 的增殖能力，表现为细胞数量和细胞活力增加，同时细胞周期蛋白 D1 和 PCNA 表达上调。同时，17β-雌二醇促进脂肪形成分化，细胞内脂质积累增加，PPARγ、ACC 和 FABP4 表达增加。值得注意的是，这些活性均因给予GPER1拮抗剂G15而明显降低，但GPER1激动剂G1增强细胞增殖和脂肪形成分化。此外，GPER1 沉默会减少细胞增殖和脂肪形成分化。同时，17β-雌二醇提高核 p-p65 的蛋白质水平。此外，p65 的磷酸化被 G1 增强，但被 G15 和 GPER1 沉默抑制。此外，p65的磷酸化是由ERK1/2介导的，表明靶向GPER1的雌激素通过ERK1/2-NF-κB信号通路调节gADSC的细胞增殖和成脂分化。该研究可为改善畜禽肉质、风味、抗寒能力提供有力的理论依据。
Adipose tissue formation and moderate fat deposition are important for the production performance and eating quality of livestock meats. The self-renewal and adipogenic differentiation of adipose-derived stem cells are responsible for the formation and development of adipose tissue. In addition, estrogen targeting G protein-coupled estrogen receptor 1 (GPER1) has been reported to modulate cell proliferation and differentiation during tissue and organ development. However, the potential correlation among estrogen, GPER1, proliferation, and adipogenic differentiation in goat adipose-derived stem cells (gADSCs) is still unclear. Herein, we demonstrated that 17β-estradiol enhances the proliferative ability of gADSCs, indicated by the increased cell number and cell viability, accompanied by up-regulated expressions of cyclin D1 and PCNA. Meanwhile, the adipogenic differentiation is promoted by 17β-estradiol, supported by higher ccumulation of intracellular lipids and increased expressions of PPARγ, ACC, and FABP4. Notably, these activities are all obviously reduced by administration with GPER1 antagonist G15, but GPER1 agonist G1 enhances cell proliferation and adipogenic differentiation. Moreover, GPER1 silencing diminishes cell proliferation and adipogenic differentiation. In parallel, 17β-estradiol elevates the protein level of nuclear p-p65. Furthermore, the phosphorylation of p65 is enhanced by G1 but inhibited by G15 and GPER1 silencing. In addition, the phosphorylation of p65 is mediated by ERK1/2, suggesting that estrogen targeting GPER1 regulates cell proliferation and adipogenic differentiation of gADSCs through the ERK1/2-NF-κB signaling pathway. This study may provide a strong theoretical basis for improving meat quality, flavor, and cold resistance of livestock.
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