Myostatin基因敲除对哺乳期幼鼠骨骼肌生长的影响

发布时间：2018-11-12 11:50

【摘要】：目的构建稳定的肌肉生长抑制素(myostatin,MSTN)基因敲除小鼠模型,观察敲除MSTN基因对哺乳期幼鼠骨骼肌生长的影响,并初步探讨其相关机制。方法采用Cre-Lox P系统建立MSTN基因敲除的小鼠模型,通过PCR法鉴定子代小鼠基因型;比较MSTN基因敲除后小鼠体质量及腿部骨骼肌质量的变化;免疫荧光法检测野生型小鼠与MSTN基因敲除小鼠腿部骨骼肌纤维横截面积;q PCR法检测MSTN基因敲除小鼠Atrogin-1和MuRF-1 mRNA的表达。结果 PCR结果显示:子代小鼠的基因型符合MSTN-lox P+/+MCK-Cre+/-;与野生型小鼠(WT)相比,MSTN敲除小鼠(KO)体质量及骨骼肌质量显著增加,在出生第7、21天差异均具有统计学意义(P0.05),腿部骨骼肌纤维显著增粗,差异具有统计学意义(P0.01);而MSTN基因敲除后小鼠Atrogin-1和MuRF-1的mRNA表达较野生型小鼠显著降低,差异具有统计学意义(P0.01)。结论利用Cre-lox P系统成功建立稳定的MSTN基因敲除的小鼠模型,该小鼠腿部骨骼肌纤维增粗,其质量以及小鼠体质量显著增加,其机制可能与泛素连接酶Atrogin-1和MuRF-1的表达下调有关。
[Abstract]:Objective to construct a stable mouse model of muscle growth inhibitor (myostatin,MSTN) gene knockout, observe the effect of knockout MSTN gene on skeletal muscle growth in lactating young rats, and explore its related mechanism. Methods the mouse model of MSTN gene knockout was established by Cre-Lox P system, and the genotypes of progeny mice were identified by PCR method, and the changes of body weight and leg skeletal muscle mass of MSTN gene knockout mice were compared. The expression of Atrogin-1 and MuRF-1 mRNA in MSTN knockout mice and wild type mice were detected by immunofluorescence method. The cross sectional area of skeletal muscle fibers in leg of wild type mice and MSTN gene knockout mice were detected by; q PCR method. Results the results of PCR showed that the genotypes of progeny mice were in line with MSTN-lox P / MCK-Cre / -; Compared with wild-type (WT) mice, the (KO) body mass and skeletal muscle mass of MSTN knockout mice were significantly increased, and the differences were statistically significant at 721 days after birth (P0.05). The difference was statistically significant (P0.01). The mRNA expression of Atrogin-1 and MuRF-1 in MSTN knockout mice was significantly lower than that in wild type mice (P0.01). Conclusion the stable mouse model of MSTN knockout was successfully established by using Cre-lox P system. The muscle fibers of the leg of the mice were thickened, the weight and the body weight of the mice were significantly increased. The mechanism may be related to the down-regulation of the expression of ubiquitin ligase Atrogin-1 and MuRF-1.
【作者单位】：第三军医大学军事预防医学院健康教育学教研室;
【基金】：国家自然科学基金面上项目(81372944)~~
【分类号】：R68

【相似文献】