摘要
细胞外基质是骨骼肌微环境的重要组成,基质中胶原蛋白的过量表达,会导致骨骼肌纤维化,因此研究miR-18a对于成肌细胞胶原蛋白表达的影响具有重要意义。利用实时荧光定量PCR、细胞划痕、组织切片苏木精-伊红染色法(hematoxylin-eosin staining, HE)染色等方法检测了肌肉损伤修复模型中miR-18a及胶原蛋白基因的表达变化以及在成肌细胞C2C12中过表达miR-18a模拟物后对胶原蛋白基因表达、细胞迁移和成肌细胞转分化的影响。结果表明,miR-18a及胶原蛋白的表达量会响应骨骼肌的损伤修复过程。在成肌细胞中,miR-18a的过表达会抑制胶原蛋白相关基因的表达。但miR-18a的过表达并不影响成肌细胞的迁移和向骨的转分化。因此miR-18a对于细胞外基质相关基因的研究,可以为骨骼肌损伤修复的治疗提供理论依据。
The extracellular matrix is an important component of the skeletal muscle microenvironment,and overexpression of collagen in the matrix leads to skeletal muscle fibrosis.Therefore,it is important to investigate the effect of miR-18a on collagen expression in myoblasts.Real-time fluorescence quantitative PCR were used to examine the changes of miR-18a and collagen gene in a muscle injury repair model.The effects of overexpression of miR-18a mimic in myoblast C2C12 on collagen gene expression,cell migration and myoblast transdifferentiation were detected by real-time quantitative PCR,cell scratching,and HE staining of tissue sections.The results show that miR-18a and collagen expression are influencing the damage repair process in skeletal muscle.In myoblasts,overexpression of miR-18a is suppressing the expression of collagen-related genes.However,miR-18a overexpression do not affect the migration and transdifferentiation of myoblasts to bone.The study of miR-18a for extracellular matrix-related genes can provide a theoretical basis for the treatment of skeletal muscle injury repair.
作者
刘戈辉
杨玉凤
刘佳夷
姜志艳
刘春城
LIU Ge-hui;YANG Yu-feng;LIU Jia-yi;JIANG Zhi-yan;LIU Chun-cheng(School of Life Science and Technology,Inner Mongolia University of Science and Technology,Baotou 014010,China;The Inner Mongolia Key Laboratory of Functional Genome Bioinformatics,Inner Mongolia University of Science and Technology,Baotou 014010,China)
出处
《科学技术与工程》
北大核心
2023年第6期2339-2346,共8页
Science Technology and Engineering
基金
国家自然科学基金(61671256,62071259)
内蒙古自治区高等学校科学研究项目(NJZY20096)
内蒙古自治区自然科学项目(2019MS08175,2021MS03007)。
关键词
细胞外基质
miR-18a
肌肉损伤修复
迁移
转分化
ECM(extracellular matrix)
miR-18a
muscle injury repair
migration
transdifferentiation
