Agricultural Ministry Key Laboratory of Swine Breeding and Genetics and Key Laboratory of Agricultural Animal Genetics, Breeding, and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, Hubei, People's Republic of China.
Mol Cell Biochem. 2012 Apr;363(1-2):291-9. doi: 10.1007/s11010-011-1181-y. Epub 2011 Dec 11.
Myostatin (MSTN) is primarily expressed in muscle and plays an important role in muscle and fat development in pigs. However, there is little information about the regulation of pig MSTN. In order to elucidate whether pig MSTN could be regulated by muscle- and fat-related factors, the porcine MSTN promoter was amplified and cloned into pGL3-basic vector, and transfected into cells to analyze the transcriptional activity of promoter with muscle- and fat-related factors through dual-luciferase reporter assays. 5'-deletion expression showed that there was a negative-regulatory region located between nucleotides -1519 and -1236 bp, and there were some positive-regulatory regions located between -1236 and -568 bp. The longest fragment (1.7 kb) was cotransfected with muscle-related transcription factor myogenic differentiation 1 (MyoD), resulting in promoter transcriptional activity upregulation. The fragment was treated by the adipogenic agents (DIM) including dexamethasone, insulin, and isobutyl-1-methylxanthine (IBMX). We found that MSTN promoter transcriptional activity can be regulated by IBMX, but not by DIM. CCAAT/enhancer binding protein (C/EBP) α and C/EBPβ, two proteins which are induced by DIM during adipogenesis were cotransfected with the 1.7-kb fragment, respectively, resulting in promoter transcriptional activity downregulation. Treating the fragment with rosiglitazone which induce the expression of peroxisome proliferator-activated receptor γ (PPARγ), resulting in promoter transcriptional activity upregulation. Cotransfection experiments confirmed this result. Taken together, we showed that porcine MSTN could be upregulated by IBMX, MyoD, and PPARγ but downregulated by C/EBPα and C/EBPβ.
肌肉生长抑制素(MSTN)主要在肌肉中表达,在猪的肌肉和脂肪发育中发挥重要作用。然而,关于猪 MSTN 的调节知之甚少。为了阐明猪 MSTN 是否可以受肌肉和脂肪相关因素的调节,扩增并克隆了猪 MSTN 启动子到 pGL3-基本载体中,并通过双荧光素酶报告基因检测分析肌肉和脂肪相关因子对启动子转录活性的影响。5'缺失表达表明,在核苷酸-1519 和-1236 bp 之间存在一个负调控区,在-1236 和-568 bp 之间存在一些正调控区。最长的片段(1.7 kb)与肌肉相关转录因子肌分化 1(MyoD)共转染,导致启动子转录活性上调。该片段用脂肪生成剂(DIM)处理,包括地塞米松、胰岛素和异丁基-1-甲基黄嘌呤(IBMX)。我们发现 MSTN 启动子转录活性可被 IBMX 调节,但不受 DIM 调节。CCAAT/增强子结合蛋白(C/EBP)α和 C/EBPβ在脂肪生成过程中被 DIM 诱导,分别与 1.7 kb 片段共转染,导致启动子转录活性下调。用罗格列酮处理该片段,可诱导过氧化物酶体增殖物激活受体γ(PPARγ)的表达,导致启动子转录活性上调。共转染实验证实了这一结果。综上所述,我们表明猪 MSTN 可被 IBMX、MyoD 和 PPARγ 上调,而被 C/EBPα 和 C/EBPβ 下调。