{"doi":"10.1016/j.cellbi.2007.05.007","title":"Myostatin and MyoD family expression in skeletal muscle of IGF‐1 knockout mice","abstract":"<jats:title>Abstract</jats:title><jats:p>Insulin‐like growth factor‐1 (IGF‐1) is a positive regulator in proliferation and differentiation of skeletal muscle cells, while myostatin (MSTN) is a member of transforming growth factor β superfamily that acts as a negative regulator of skeletal muscle mass. The present study was performed to detail whether a correlation exists between MSTN and IGF‐1 in skeletal muscle of IGF‐1 knockout mice (IGF‐1<jats:sup>−/−</jats:sup>) and their wild type (WT; i.e., IGF‐1<jats:sup>+/+</jats:sup>) littermates. The body weight of IGF‐1<jats:sup>−/−</jats:sup> animals was 32% that of WT littermates. The fiber cross‐sectional areas (CSA) and number of fibers in <jats:italic>M. rectus femoris</jats:italic> of IGF‐1<jats:sup>−/−</jats:sup> animals were 49 and 59% those of WT animals, respectively. Thus, muscle hypoplasia of IGF‐1<jats:sup>−/−</jats:sup> undoubtedly was confirmed. Myostatin mRNA levels and protein levels were similar between <jats:italic>M. gastrocnemius</jats:italic> of IGF‐1<jats:sup>−/−</jats:sup> and WT animals. Myostatin immunoreactivity was similarly localized in muscle fibers of both IGF‐1<jats:sup>−/−</jats:sup> and WT <jats:italic>M. rectus femoris</jats:italic>. The mRNA levels of MyoD family (Myf5, MyoD, MRF4, myogenin) were differentially expressed in IGF‐1<jats:sup>−/−</jats:sup> <jats:italic>M. gastrocnemius</jats:italic>, in which the mRNA expression of MRF4 and myogenin was significantly lower, whereas there were no changes in the mRNA expression of Myf5 and MyoD. These findings first describe that myostatin expression is not influenced by intrinsic failure of IGF‐1, although MRF4 and myogenin are downregulated.</jats:p>","journal":"Cell Biology International","year":2007,"id":613188,"datarank":0.5416376868966337,"base_score":3.6109179126442243,"endowment":3.6109179126442243,"self_citation_contribution":0.5416376868966337,"citation_network_contribution":0.0,"self_endowment_contribution":0.5416376868966337,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":36,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1539495,"name":"Shinichiro Hayashi","orcid":null,"position":1,"is_corresponding":false},{"id":153043,"name":"Tomomi Sato","orcid":null,"position":2,"is_corresponding":false},{"id":1579531,"name":"Yoshikazu Taketa","orcid":null,"position":3,"is_corresponding":false},{"id":942468,"name":"Kouichi Watanabe","orcid":null,"position":4,"is_corresponding":false},{"id":1579532,"name":"Shinji Hayashi","orcid":null,"position":5,"is_corresponding":false},{"id":1579533,"name":"Sachi Tanaka","orcid":null,"position":6,"is_corresponding":false},{"id":1579534,"name":"Shyuichi Ohwada","orcid":null,"position":7,"is_corresponding":false},{"id":941871,"name":"Hisashi Aso","orcid":"0000-0001-5114-4651","position":8,"is_corresponding":false},{"id":1034893,"name":"Takahiro Yamaguchi","orcid":"0000-0003-3140-1344","position":9,"is_corresponding":false},{"id":140793,"name":"Masato Miyake","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Myostatin and MyoD family expression in skeletal muscle of IGF‐1 knockout mice","abstract":"<jats:title>Abstract</jats:title><jats:p>Insulin‐like growth factor‐1 (IGF‐1) is a positive regulator in proliferation and differentiation of skeletal muscle cells, while myostatin (MSTN) is a member of transforming growth factor β superfamily that acts as a negative regulator of skeletal muscle mass. The present study was performed to detail whether a correlation exists between MSTN and IGF‐1 in skeletal muscle of IGF‐1 knockout mice (IGF‐1<jats:sup>−/−</jats:sup>) and their wild type (WT; i.e., IGF‐1<jats:sup>+/+</jats:sup>) littermates. The body weight of IGF‐1<jats:sup>−/−</jats:sup> animals was 32% that of WT littermates. The fiber cross‐sectional areas (CSA) and number of fibers in <jats:italic>M. rectus femoris</jats:italic> of IGF‐1<jats:sup>−/−</jats:sup> animals were 49 and 59% those of WT animals, respectively. Thus, muscle hypoplasia of IGF‐1<jats:sup>−/−</jats:sup> undoubtedly was confirmed. Myostatin mRNA levels and protein levels were similar between <jats:italic>M. gastrocnemius</jats:italic> of IGF‐1<jats:sup>−/−</jats:sup> and WT animals. Myostatin immunoreactivity was similarly localized in muscle fibers of both IGF‐1<jats:sup>−/−</jats:sup> and WT <jats:italic>M. rectus femoris</jats:italic>. The mRNA levels of MyoD family (Myf5, MyoD, MRF4, myogenin) were differentially expressed in IGF‐1<jats:sup>−/−</jats:sup> <jats:italic>M. gastrocnemius</jats:italic>, in which the mRNA expression of MRF4 and myogenin was significantly lower, whereas there were no changes in the mRNA expression of Myf5 and MyoD. These findings first describe that myostatin expression is not influenced by intrinsic failure of IGF‐1, although MRF4 and myogenin are downregulated.</jats:p>","is_dataset_classified":null,"base_score":3.6109179126442243,"endowment":3.6109179126442243,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"17590360","pmcid":null,"openalex_id":"https://openalex.org/W2079826520","authors":[],"funders":[],"total_grants":0,"fwci":0.7994,"citation_percentile":0.71149805,"influential_citations":0,"citation_trend":[{"year":2012,"count":2},{"year":2013,"count":2},{"year":2014,"count":3},{"year":2015,"count":1},{"year":2016,"count":1},{"year":2017,"count":1},{"year":2018,"count":2},{"year":2019,"count":2},{"year":2020,"count":1},{"year":2021,"count":1},{"year":2022,"count":1},{"year":2023,"count":1},{"year":2024,"count":6},{"year":2025,"count":1},{"year":2026,"count":1}],"oa_status":"closed","license":"http://onlinelibrary.wiley.com/termsAndConditions#vor","oa_locations":[{"url":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1016%2Fj.cellbi.2007.05.007","host_type":"publisher"},{"url":"https://onlinelibrary.wiley.com/doi/pdf/10.1016/j.cellbi.2007.05.007","host_type":"publisher"},{"url":"https://doi.org/10.1016/j.cellbi.2007.05.007","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/17590360","host_type":"repository"}],"fields_of_study":["Muscle Physiology and Disorders","Muscle metabolism and nutrition","Growth Hormone and Insulin-like Growth Factors","Animals","Insulin-Like Growth Factor I","Male","Mice","Mice, Knockout","Muscle Strength","Muscle, Skeletal","MyoD Protein","Myogenic Regulatory Factor 5","Myogenic Regulatory Factors","Myogenin","Myostatin","RNA, Messenger","Reverse Transcriptase Polymerase Chain Reaction","Transforming Growth Factor beta"],"mesh_terms":["Animals","Insulin-Like Growth Factor I","Male","RNA, Messenger","Transforming Growth Factor beta","MyoD Protein","Myogenic Regulatory Factors","Myogenin","Mice, Knockout","Muscle, Skeletal","Reverse Transcriptase Polymerase Chain Reaction","Mice","Myogenic Regulatory Factor 5","Muscle Strength","Myostatin"],"keywords":["Myostatin","Myogenin","MyoD","MYF5","Endocrinology","Internal medicine","Skeletal muscle","Myogenic regulatory factors","Biology","Growth differentiation factor","Follistatin","Myogenesis","Medicine","Genetics","Gene"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-02T07:00:34.427462Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}