Matches in SemOpenAlex for { <https://semopenalex.org/work/W2034569221> ?p ?o ?g. }
- W2034569221 endingPage "297" @default.
- W2034569221 startingPage "286" @default.
- W2034569221 abstract "Abstract OPN is an ECM protein with diverse localization and functionality. The role of OPN during fracture healing was examined using wildtype and OPN −/− mice. Results showed that OPN plays an important role in regulation of angiogenesis, callus formation, and mechanical strength in early stages of healing and facilitates late stage bone remodeling and ECM organization. Introduction : Osteopontin (OPN) is an extracellular matrix (ECM) protein with diverse localization and functionality that has been reported to play a regulatory role in both angiogenesis and osteoclastic bone remodeling, two vital processes for normal bone healing. Materials and Methods : Bone repair in wildtype and OPN −/− mice was studied using a femoral fracture model. μCT was used for quantitative angiographic measurements at 7 and 14 days and to assess callus size and mineralization at 7, 14, 28, and 56 days. Biomechanical testing was performed on intact bones and on fracture specimens at 14, 28, and 56 days. Histology and quantitative RT‐PCR were used to evaluate cellular functions related to ECM formation and bone remodeling. Results : OPN deficiency was validated in the OPN −/− mice, which generally displayed normal levels of related ECM proteins. Intact OPN −/− bones displayed increased elastic modulus but decreased strength and ductility. Fracture neovascularization was reduced at 7 but not 14 days in OPN −/− mice. OPN −/− mice exhibited smaller fracture calluses at 7 and 14 days, as well as lower maximum torque and work to failure. At 28 days, OPN −/− mice had normal callus size but a persistent reduction in maximum torque and work to failure. Osteoclast differentiation occurred normally, but mature osteoclasts displayed reduced functionality, decreasing late stage remodeling in OPN −/− mice. Thus, at 56 days, OPN −/− fractures possessed increased callus volume, increased mechanical stiffness, and altered collagen fiber organization. Conclusions : This study showed multiple, stage‐dependent roles of OPN during fracture healing. We conclude that OPN deficiency alters the functionality of multiple cell types, resulting in delayed early vascularization, altered matrix organization and late remodeling, and reduced biomechanical properties. These findings contribute to an improved understanding of the role of OPN in vivo and provide new insight into mechanistic control of vascularization and bone regeneration during fracture repair." @default.
- W2034569221 created "2016-06-24" @default.
- W2034569221 creator A5008872627 @default.
- W2034569221 creator A5016501769 @default.
- W2034569221 creator A5075794128 @default.
- W2034569221 creator A5080019571 @default.
- W2034569221 creator A5086186521 @default.
- W2034569221 date "2007-02-01" @default.
- W2034569221 modified "2023-10-16" @default.
- W2034569221 title "Impaired Angiogenesis, Early Callus Formation, and Late Stage Remodeling in Fracture Healing of Osteopontin-Deficient Mice" @default.
- W2034569221 cites W1839610592 @default.
- W2034569221 cites W1912515756 @default.
- W2034569221 cites W1977577042 @default.
- W2034569221 cites W1979242330 @default.
- W2034569221 cites W1987504060 @default.
- W2034569221 cites W1990289437 @default.
- W2034569221 cites W1993255160 @default.
- W2034569221 cites W1993917627 @default.
- W2034569221 cites W2008675789 @default.
- W2034569221 cites W2014097308 @default.
- W2034569221 cites W2014732354 @default.
- W2034569221 cites W2033316320 @default.
- W2034569221 cites W2034378488 @default.
- W2034569221 cites W2034462747 @default.
- W2034569221 cites W2035572527 @default.
- W2034569221 cites W2039659007 @default.
- W2034569221 cites W2041287210 @default.
- W2034569221 cites W2043033796 @default.
- W2034569221 cites W2046119439 @default.
- W2034569221 cites W2051055532 @default.
- W2034569221 cites W2053286268 @default.
- W2034569221 cites W2055502077 @default.
- W2034569221 cites W2068996375 @default.
- W2034569221 cites W2072508323 @default.
- W2034569221 cites W2103492381 @default.
- W2034569221 cites W2116257804 @default.
- W2034569221 cites W2116643539 @default.
- W2034569221 cites W2117729857 @default.
- W2034569221 cites W2121793520 @default.
- W2034569221 cites W2128695989 @default.
- W2034569221 cites W2134771161 @default.
- W2034569221 cites W2139996507 @default.
- W2034569221 cites W2151615254 @default.
- W2034569221 cites W2161630702 @default.
- W2034569221 cites W2162664959 @default.
- W2034569221 cites W2165916469 @default.
- W2034569221 cites W2168609932 @default.
- W2034569221 cites W2168789685 @default.
- W2034569221 cites W2988335631 @default.
- W2034569221 doi "https://doi.org/10.1359/jbmr.061103" @default.
- W2034569221 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17087627" @default.
- W2034569221 hasPublicationYear "2007" @default.
- W2034569221 type Work @default.
- W2034569221 sameAs 2034569221 @default.
- W2034569221 citedByCount "184" @default.
- W2034569221 countsByYear W20345692212012 @default.
- W2034569221 countsByYear W20345692212013 @default.
- W2034569221 countsByYear W20345692212014 @default.
- W2034569221 countsByYear W20345692212015 @default.
- W2034569221 countsByYear W20345692212016 @default.
- W2034569221 countsByYear W20345692212017 @default.
- W2034569221 countsByYear W20345692212018 @default.
- W2034569221 countsByYear W20345692212019 @default.
- W2034569221 countsByYear W20345692212020 @default.
- W2034569221 countsByYear W20345692212021 @default.
- W2034569221 countsByYear W20345692212022 @default.
- W2034569221 countsByYear W20345692212023 @default.
- W2034569221 crossrefType "journal-article" @default.
- W2034569221 hasAuthorship W2034569221A5008872627 @default.
- W2034569221 hasAuthorship W2034569221A5016501769 @default.
- W2034569221 hasAuthorship W2034569221A5075794128 @default.
- W2034569221 hasAuthorship W2034569221A5080019571 @default.
- W2034569221 hasAuthorship W2034569221A5086186521 @default.
- W2034569221 hasBestOaLocation W20345692211 @default.
- W2034569221 hasConcept C105702510 @default.
- W2034569221 hasConcept C126322002 @default.
- W2034569221 hasConcept C134018914 @default.
- W2034569221 hasConcept C142724271 @default.
- W2034569221 hasConcept C170033053 @default.
- W2034569221 hasConcept C185592680 @default.
- W2034569221 hasConcept C189165786 @default.
- W2034569221 hasConcept C202751555 @default.
- W2034569221 hasConcept C2778260815 @default.
- W2034569221 hasConcept C2780394083 @default.
- W2034569221 hasConcept C2780804394 @default.
- W2034569221 hasConcept C54355233 @default.
- W2034569221 hasConcept C55493867 @default.
- W2034569221 hasConcept C71924100 @default.
- W2034569221 hasConcept C8337478 @default.
- W2034569221 hasConcept C86803240 @default.
- W2034569221 hasConcept C95444343 @default.
- W2034569221 hasConcept C9549007 @default.
- W2034569221 hasConceptScore W2034569221C105702510 @default.
- W2034569221 hasConceptScore W2034569221C126322002 @default.
- W2034569221 hasConceptScore W2034569221C134018914 @default.
- W2034569221 hasConceptScore W2034569221C142724271 @default.
- W2034569221 hasConceptScore W2034569221C170033053 @default.
- W2034569221 hasConceptScore W2034569221C185592680 @default.