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http://purl.uniprot.org/citations/32360587http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32360587http://www.w3.org/2000/01/rdf-schema#comment"Bone fracture is accompanied by trauma, mechanical stresses, and inflammation - conditions known to induce the mitochondrial permeability transition. This phenomenon occurs due to opening of the mitochondrial permeability transition pore (MPTP) promoted by cyclophilin D (CypD). MPTP opening leads to more inflammation, cell death and potentially to disruption of fracture repair. Here we performed a proof-of-concept study and tested a hypothesis that protecting mitochondria from MPTP opening via inhibition of CypD improves fracture repair. First, our in vitro experiments indicated pro-osteogenic and anti-inflammatory effects in osteoprogenitors upon CypD knock-out or pharmacological inhibition. Using a bone fracture model in mice, we observed that bone formation and biomechanical properties of repaired bones were significantly increased in CypD knock-out mice or wild type mice treated with a CypD inhibitor, NIM811, when compared to controls. These effects were evident in young male but not female mice, however in older (13 month-old) female mice bone formation was also increased during fracture repair. In contrast to global CypD knock-out, mesenchymal lineage-specific (Prx1-Cre driven) CypD deletion did not result in improved fracture repair. Our findings implicate MPTP in bone fracture and suggest systemic CypD inhibition as a modality to promote fracture repair."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.org/dc/terms/identifier"doi:10.1016/j.bone.2020.115391"xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Huber A."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Smith C.O."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Brown E."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Eliseev R.A."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Schilling K."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Awad H."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Sheu T.J."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Paine A."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Shum L.C."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Shares B.H."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Gira E."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/author"Sautchuk R. Jr."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/name"Bone"xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/pages"115391"xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/title"Inhibition of the mitochondrial permeability transition improves bone fracture repair."xsd:string
http://purl.uniprot.org/citations/32360587http://purl.uniprot.org/core/volume"137"xsd:string
http://purl.uniprot.org/citations/32360587http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32360587
http://purl.uniprot.org/citations/32360587http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32360587
http://purl.uniprot.org/uniprot/#_Q99KR7-mappedCitation-32360587http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32360587
http://purl.uniprot.org/uniprot/Q99KR7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32360587