Wen Fengyun, Zheng Jin, Yu Jing, Gao Mingju, Gao Sumin, Zhou Yingying, Liu Jianyu, Yang Zaiqing
a Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Life Science and Technology , Huazhong Agricultural University , Wuhan , PR China.
b College of Animal Science and Technology , Henan University of Science and Technology , Luoyang , PR China.
Biosci Biotechnol Biochem. 2016 Jul;80(7):1313-20. doi: 10.1080/09168451.2016.1153951. Epub 2016 Feb 29.
Obesity is documented to be a state of chronic mild inflammation associated with increased macrophage infiltration into adipose tissue and liver and skeletal muscle. As a pleiotropic inflammatory mediator, macrophage migration inhibitory factor (MIF) is associated with metabolic disease, so MIF may signal molecular links between adipocytes and myocytes. MIF expression was modified during myoblast differentiation, but the role of MIF during this process is unclear. C2C12 cells were transfected with MIF to investigate their role during differentiation. MIF expression attenuated C2C12 differentiation. It did not change proliferation, but downregulated cyclin D1 and CDK4, causing cell accumulation in the G1 phase. p21 protein was increased significantly and MyoD, MyoG, and p21 mRNA also increased significantly in the C2C12 cells treated with ISO-1, suggesting that inhibition of MIF promotes differentiation. MIF inhibits the myoblast differentiation by affecting the cell cycle progression, but does not affect proliferation.
肥胖被证明是一种慢性轻度炎症状态，与巨噬细胞浸润到脂肪组织、肝脏和骨骼肌增加有关。作为一种多效性炎症介质，巨噬细胞移动抑制因子（MIF）与代谢疾病相关，因此MIF可能是脂肪细胞和肌细胞之间的分子联系信号。成肌细胞分化过程中MIF表达发生改变，但MIF在此过程中的作用尚不清楚。用MIF转染C2C12细胞以研究其在分化过程中的作用。MIF表达减弱了C2C12细胞的分化。它不改变增殖，但下调细胞周期蛋白D1和细胞周期蛋白依赖性激酶4（CDK4），导致细胞在G1期积累。在用ISO-1处理的C2C12细胞中，p21蛋白显著增加，MyoD、MyoG和p21 mRNA也显著增加，这表明抑制MIF可促进分化。MIF通过影响细胞周期进程抑制成肌细胞分化，但不影响增殖。
