Chuncheng Liu, Yuxin Cao, Lei Li, Yiting Wang, Qingyong Meng
{"title":"过表达miR-29ab1簇通过抑制Mstn导致1月龄小鼠肌肉过度生长。","authors":"Chuncheng Liu, Yuxin Cao, Lei Li, Yiting Wang, Qingyong Meng","doi":"10.1089/dna.2022.0247","DOIUrl":null,"url":null,"abstract":"Skeletal muscle mass is closely related to strength and health. Multiple genes and signaling pathways are involved in the regulation of skeletal muscle hypertrophy. miR-29 can participate in various processes of skeletal muscle development through different target genes. However, studies are needed on the function of miR-29 in skeletal muscle during mouse puberty. We used mice in which overexpression of miR-29ab1 cluster could be induced specifically within skeletal muscle, and investigated the effects of miR-29 overexpression on skeletal muscle at 1 month of age. We found that the overexpression of miR-29ab1 cluster in juvenile mice caused skeletal muscle mass and myofiber cross-sectional area to increase. The study on the mechanism of miR-29 inducing skeletal muscle hypertrophy had found that miR-29 achieved its function by inhibiting the expression of Mstn. At the same time, injured myofibers were present within miR-29ab1 cluster overexpressing skeletal muscle. The damage of skeletal muscle may be due to the inhibition of the type IV collagen by miR-29. These results indicate that although the overexpression of miR-29ab1 cluster can induce skeletal muscle hypertrophy in mouse juvenile, it simultaneously causes skeletal muscle damage.","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":"42 1","pages":"43-52"},"PeriodicalIF":2.6000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Overexpression of miR-29ab1 Cluster Results in Excessive Muscle Growth in 1-Month-old Mice by Inhibiting <i>Mstn</i>.\",\"authors\":\"Chuncheng Liu, Yuxin Cao, Lei Li, Yiting Wang, Qingyong Meng\",\"doi\":\"10.1089/dna.2022.0247\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Skeletal muscle mass is closely related to strength and health. Multiple genes and signaling pathways are involved in the regulation of skeletal muscle hypertrophy. miR-29 can participate in various processes of skeletal muscle development through different target genes. However, studies are needed on the function of miR-29 in skeletal muscle during mouse puberty. We used mice in which overexpression of miR-29ab1 cluster could be induced specifically within skeletal muscle, and investigated the effects of miR-29 overexpression on skeletal muscle at 1 month of age. We found that the overexpression of miR-29ab1 cluster in juvenile mice caused skeletal muscle mass and myofiber cross-sectional area to increase. The study on the mechanism of miR-29 inducing skeletal muscle hypertrophy had found that miR-29 achieved its function by inhibiting the expression of Mstn. At the same time, injured myofibers were present within miR-29ab1 cluster overexpressing skeletal muscle. The damage of skeletal muscle may be due to the inhibition of the type IV collagen by miR-29. These results indicate that although the overexpression of miR-29ab1 cluster can induce skeletal muscle hypertrophy in mouse juvenile, it simultaneously causes skeletal muscle damage.\",\"PeriodicalId\":11248,\"journal\":{\"name\":\"DNA and cell biology\",\"volume\":\"42 1\",\"pages\":\"43-52\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"DNA and cell biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1089/dna.2022.0247\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"DNA and cell biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1089/dna.2022.0247","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Overexpression of miR-29ab1 Cluster Results in Excessive Muscle Growth in 1-Month-old Mice by Inhibiting Mstn.
Skeletal muscle mass is closely related to strength and health. Multiple genes and signaling pathways are involved in the regulation of skeletal muscle hypertrophy. miR-29 can participate in various processes of skeletal muscle development through different target genes. However, studies are needed on the function of miR-29 in skeletal muscle during mouse puberty. We used mice in which overexpression of miR-29ab1 cluster could be induced specifically within skeletal muscle, and investigated the effects of miR-29 overexpression on skeletal muscle at 1 month of age. We found that the overexpression of miR-29ab1 cluster in juvenile mice caused skeletal muscle mass and myofiber cross-sectional area to increase. The study on the mechanism of miR-29 inducing skeletal muscle hypertrophy had found that miR-29 achieved its function by inhibiting the expression of Mstn. At the same time, injured myofibers were present within miR-29ab1 cluster overexpressing skeletal muscle. The damage of skeletal muscle may be due to the inhibition of the type IV collagen by miR-29. These results indicate that although the overexpression of miR-29ab1 cluster can induce skeletal muscle hypertrophy in mouse juvenile, it simultaneously causes skeletal muscle damage.
期刊介绍:
DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward.
DNA and Cell Biology coverage includes:
Gene Structure, Function, and Regulation
Gene regulation
Molecular mechanisms of cell activation
Mechanisms of transcriptional, translational, or epigenetic control of gene expression
Molecular Medicine
Molecular pathogenesis
Genetic approaches to cancer and autoimmune diseases
Translational studies in cell and molecular biology
Cellular Organelles
Autophagy
Apoptosis
P bodies
Peroxisosomes
Protein Biosynthesis and Degradation
Regulation of protein synthesis
Post-translational modifications
Control of degradation
Cell-Autonomous Inflammation and Host Cell Response to Infection
Responses to cytokines and other physiological mediators
Evasive pathways of pathogens.