Uncoupling protein 1 (UCP1) is responsible for non‐shivering thermogenesis, with restricted expression in brown/beige adipocytes in humans and rodents. We have previously shown an unexpected expression of UCP1 in bovine skeletal muscles. This study evaluated factors affecting Ucp1 gene expression in cultured bovine myogenic cells. Myosatellite cells, which were isolated from the bovine musculus longissimus cervicis, were induced to differentiate into myotubes in the presence of 2% horse serum. Previous studies using murine brown/beige adipocytes revealed that Ucp1 expression levels are directly increased by forskolin and all‐trans retinoic acid (RA). The transforming growth factor‐β (TGF‐β)/activin pathway negatively regulated Ucp1 expression, whereas activation of the bone morphogenetic protein (BMP) pathway indirectly increases Ucp1 expression through the stimulation of brown/beige adipogenesis. Neither forskolin nor RA significantly affected Ucp1 mRNA levels in bovine myogenic cells. A‐83‐01, an inhibitor of the TGF‐β/activin pathway, stimulated myogenesis in these cells. A‐83‐01 significantly increased the expression of some brown fat signature genes such as Pgc‐1α, Cox7a1, and Dio2, with a quantitative but not significant increase in the expression of Ucp1. Treatment with LDN‐193189, an inhibitor of the BMP pathway, did not affect the differentiation of bovine myosatellite cells. Rather, LDN‐193189 increased Ucp1 mRNA levels without modulating the levels of other brown/beige adipocyte‐related genes. The current results indicate that the regulation of Ucp1 expression in bovine myogenic cells is distinct from that in murine brown/beige adipocytes, which has been more intensely characterized.

中文翻译：

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牛肌原细胞中转化生长因子β家族的内源性活性调节解偶联蛋白1及其相关基因的表达

解偶联蛋白1（UCP1）负责非发抖的生热作用，在人类和啮齿类动物的棕色/米色脂肪细胞中表达受限。我们以前已经显示出UCP1在牛骨骼肌中出乎意料的表达。这项研究评估了影响培养牛肌原细胞中Ucp1基因表达的因素。Myosatellite细胞，其是从牛分离家鼠最长cervicis，被诱导分化成肌管在2％马血清的存在。以前使用鼠棕色/米色脂肪细胞进行的研究表明，毛喉素和全反式维甲酸（RA）直接增加了Ucp1的表达水平。转化生长因子-β（TGF-β）/激活素途径负调控Ucp1表达，而骨形态发生蛋白（BMP）途径的激活通过刺激棕色/米色脂肪形成间接增加Ucp1表达。福司可林和RA均未显着影响牛成肌细胞中Ucp1 mRNA的水平。TGF-β/激活素途径的抑制剂A-83-01刺激了这些细胞的肌发生。A-83-01显著增加的一些棕色脂肪签名基因，诸如表达PGC-1α，Cox7a1，和DIO2，与表达的定量，但不增加显著UCP1。用BMP途径抑制剂LDN-193189进行的治疗不会影响牛异卫星细胞的分化。相反，LDN‐193189可增加Ucp1 mRNA水平，而不会调节其他棕色/米色脂肪细胞相关基因的水平。目前的结果表明，Ucp1在牛成肌细胞中的表达调控与在鼠棕色/米色脂肪细胞中的调控不同，后者具有更强的特征。