{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang L"],"funding":["National Institute of Arthritis and Musculoskeletal and Skin Diseases","American Heart Association","NIDDK NIH HHS","American Heart Association-American Stroke Association","NIAMS NIH HHS","NIH HHS"],"pagination":["2229-2242"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8865375"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["36(11)"],"pubmed_abstract":["Defective or insufficient bone repair and regeneration are common in patients as a result of major trauma or severe disease. Cell therapy with periosteal mesenchymal progenitors, which can be limited in severe injury, serves as a promising approach; however, its efficacy is limited due to a repair-hostile ischemic tissue microenvironment after traumatic fracture. Here we report that plasminogen (Plg), a factor that is upregulated in these environments, is critical for fracture healing. Plg knockout mice had impaired trabecular and cortical bone structure and exhibited delayed and incomplete fracture healing. Interestingly, Plg deficiency greatly reduced the thickness of expanded periosteum, suggesting a role of Plg in periosteal mesenchymal progenitor-mediated bone repair. In culture, Plg "],"journal":["Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research"],"pubmed_title":["Plasminogen Regulates Fracture Repair by Promoting the Functions of Periosteal Mesenchymal Progenitors."],"pmcid":["PMC8865375"],"funding_grant_id":["P30 AR069619","R01 AR066098","R01AR066098","17GRNT33650029","P30AR069619","R01DK095803","R01 DK095803"],"pubmed_authors":["Yao L","Fan Y","Qin L","He Z","Ahn J","Zhang R","Gong Y","Duan H","Yang F","Lin M","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"Plasminogen Regulates Fracture Repair by Promoting the Functions of Periosteal Mesenchymal Progenitors.","description":"Defective or insufficient bone repair and regeneration are common in patients as a result of major trauma or severe disease. Cell therapy with periosteal mesenchymal progenitors, which can be limited in severe injury, serves as a promising approach; however, its efficacy is limited due to a repair-hostile ischemic tissue microenvironment after traumatic fracture. Here we report that plasminogen (Plg), a factor that is upregulated in these environments, is critical for fracture healing. Plg knockout mice had impaired trabecular and cortical bone structure and exhibited delayed and incomplete fracture healing. Interestingly, Plg deficiency greatly reduced the thickness of expanded periosteum, suggesting a role of Plg in periosteal mesenchymal progenitor-mediated bone repair. In culture, Plg ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2025-04-03T22:45:12.984Z","creation":"2025-02-19T01:30:35.458Z"},"accession":"S-EPMC8865375","cross_references":{"pubmed":["34378815"],"doi":["10.1002/jbmr.4423"]}}