FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2772476487> ?p ?o ?g. }

• W2772476487 endingPage "366" @default.
• W2772476487 startingPage "365" @default.
• W2772476487 abstract "To the Editor: We read with great interest the recent article in the Journal of Bone and Mineral Research by Convente and colleagues, “Depletion of mast cells and macrophages impairs heterotopic ossification in an Acvr1R206H mouse model of fibrodysplasia ossificans progressiva.”1 This article reports that muscle injury caused by intramuscular injection of cardiotoxin from Naja mossambica mossambica venom into the Acvr1R206H mouse causes the development of heterotopic ossifications (HO) at the injury site. They demonstrated exacerbated macrophage and mast cell accumulation in Acvr1R206H mice and showed that depletion of macrophages in vivo with clodronate-loaded liposomes, genetic impairment of mast cells, or a combination of both approaches substantially reduced the volume of HO. The authors conclude that the immune system, particularly macrophages and mast cells, are major contributors to the initiation and development of HO in fibrodysplasia ossificans progressiva (FOP). This finding of macrophage involvement in the development of HO in FOP is wholly consistent with our previously published work using identical methodology to show that macrophages mediate the development of HO in wild-type mice with spinal cord injury (SCI).2 In that work, we showed that the combination of SCI with intramuscular injection of cardiotoxin from Naja mossambica mossambica venom causes development of neurogenic HO in wild-type mice. The development of HO in SCI mice recapitulated the clinical features of neurogenic HO in patients with SCI or traumatic brain injury. We also showed that concomitant depletion of macrophages in vivo, using clodronate-loaded liposomes, dramatically reduced the volume of HO in this model of neurogenic HO after SCI.2 Convente and colleagues suggest that Substance P, as a neuroinflammatory modulator, may be a major molecular driver of HO. We reported significantly elevated Substance P in serum of patients with neurogenic HO, but that Substance P antagonism was modestly protective in the neurogenic HO mouse model.2 We concluded that macrophages are key drivers of neurogenic HO in this model. The role of macrophages in promoting bone formation in HO, both in our model of trauma-induced HO and in Convente and colleagues’ Acvr1 mutant model of HO in FOP,1 is consistent with our previously published work showing a key role of macrophages in the maintenance of functional osteoblasts, bone formation, and bone repair.3-6 We have now identified that the range of cytokines induced in macrophages by cardiotoxin injection includes oncostatin M, and secretion of oncostatin M by inflammatory monocytes and macrophages infiltrating the injured muscle is a key driver of HO development and formation of heterotopic hematopoietic stem cell niches in humans and mice with SCI.7 In conclusion, we wish to highlight a point that seems to have been overlooked by Convente and colleagues, which is that even though HO development in these two clinically distinct situations (genetically-driven FOP versus trauma-driven neurogenic HO) might be expected to have distinct mechanisms, the use of overlapping methods to interrogate these two models revealed that cytokine production by macrophages is a common underlying cause and thus represents a potential therapeutic strategy for both conditions. All authors state that they have no conflicts of interest. Work cited in this letter was supported in part by project grant 1101620 from the French Government Defense Procurement and Technology Agency (DGA; to FT, FG, JJL, and MCLBK), project grant APP1101620 from the National Health and Medical Research Council of Australia (NHMRC to JPL, AP, FG, and NAS), and award W81XWH-15-1-0606 from the Spinal Cord Injury Research Program of the US Department of Defense. JPL is supported by research fellowship APP1044091 from the NHMRC." @default.
• W2772476487 created "2017-12-22" @default.
• W2772476487 creator A5030167860 @default.
• W2772476487 creator A5034604471 @default.
• W2772476487 creator A5043878576 @default.
• W2772476487 creator A5053223017 @default.
• W2772476487 creator A5072162686 @default.
• W2772476487 creator A5082442667 @default.
• W2772476487 creator A5087957815 @default.
• W2772476487 creator A5088093065 @default.
• W2772476487 creator A5090515811 @default.
• W2772476487 date "2017-12-27" @default.
• W2772476487 modified "2023-10-18" @default.
• W2772476487 title "<b>Macrophages</b> Driving Heterotopic Ossification: Convergence of Genetically-Driven and Trauma-Driven Mechanisms" @default.
• W2772476487 cites W1555097282 @default.
• W2772476487 cites W1802397357 @default.
• W2772476487 cites W2109525494 @default.
• W2772476487 cites W2150362511 @default.
• W2772476487 cites W2762933082 @default.
• W2772476487 cites W2766555128 @default.
• W2772476487 cites W2766645907 @default.
• W2772476487 doi "https://doi.org/10.1002/jbmr.3346" @default.
• W2772476487 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29178621" @default.
• W2772476487 hasPublicationYear "2017" @default.
• W2772476487 type Work @default.
• W2772476487 sameAs 2772476487 @default.
• W2772476487 citedByCount "15" @default.
• W2772476487 countsByYear W27724764872019 @default.
• W2772476487 countsByYear W27724764872020 @default.
• W2772476487 countsByYear W27724764872021 @default.
• W2772476487 countsByYear W27724764872022 @default.
• W2772476487 countsByYear W27724764872023 @default.
• W2772476487 crossrefType "journal-article" @default.
• W2772476487 hasAuthorship W2772476487A5030167860 @default.
• W2772476487 hasAuthorship W2772476487A5034604471 @default.
• W2772476487 hasAuthorship W2772476487A5043878576 @default.
• W2772476487 hasAuthorship W2772476487A5053223017 @default.
• W2772476487 hasAuthorship W2772476487A5072162686 @default.
• W2772476487 hasAuthorship W2772476487A5082442667 @default.
• W2772476487 hasAuthorship W2772476487A5087957815 @default.
• W2772476487 hasAuthorship W2772476487A5088093065 @default.
• W2772476487 hasAuthorship W2772476487A5090515811 @default.
• W2772476487 hasBestOaLocation W27724764871 @default.
• W2772476487 hasConcept C105702510 @default.
• W2772476487 hasConcept C126322002 @default.
• W2772476487 hasConcept C142724271 @default.
• W2772476487 hasConcept C150903083 @default.
• W2772476487 hasConcept C202751555 @default.
• W2772476487 hasConcept C203014093 @default.
• W2772476487 hasConcept C207001950 @default.
• W2772476487 hasConcept C2777995074 @default.
• W2772476487 hasConcept C2778842504 @default.
• W2772476487 hasConcept C2779244956 @default.
• W2772476487 hasConcept C2779726688 @default.
• W2772476487 hasConcept C2779959927 @default.
• W2772476487 hasConcept C2780650075 @default.
• W2772476487 hasConcept C2909145422 @default.
• W2772476487 hasConcept C55493867 @default.
• W2772476487 hasConcept C71924100 @default.
• W2772476487 hasConcept C86803240 @default.
• W2772476487 hasConceptScore W2772476487C105702510 @default.
• W2772476487 hasConceptScore W2772476487C126322002 @default.
• W2772476487 hasConceptScore W2772476487C142724271 @default.
• W2772476487 hasConceptScore W2772476487C150903083 @default.
• W2772476487 hasConceptScore W2772476487C202751555 @default.
• W2772476487 hasConceptScore W2772476487C203014093 @default.
• W2772476487 hasConceptScore W2772476487C207001950 @default.
• W2772476487 hasConceptScore W2772476487C2777995074 @default.
• W2772476487 hasConceptScore W2772476487C2778842504 @default.
• W2772476487 hasConceptScore W2772476487C2779244956 @default.
• W2772476487 hasConceptScore W2772476487C2779726688 @default.
• W2772476487 hasConceptScore W2772476487C2779959927 @default.
• W2772476487 hasConceptScore W2772476487C2780650075 @default.
• W2772476487 hasConceptScore W2772476487C2909145422 @default.
• W2772476487 hasConceptScore W2772476487C55493867 @default.
• W2772476487 hasConceptScore W2772476487C71924100 @default.
• W2772476487 hasConceptScore W2772476487C86803240 @default.
• W2772476487 hasFunder F4320334705 @default.
• W2772476487 hasIssue "2" @default.
• W2772476487 hasLocation W27724764871 @default.
• W2772476487 hasLocation W27724764872 @default.
• W2772476487 hasLocation W27724764873 @default.
• W2772476487 hasOpenAccess W2772476487 @default.
• W2772476487 hasPrimaryLocation W27724764871 @default.
• W2772476487 hasRelatedWork W147401788 @default.
• W2772476487 hasRelatedWork W180266173 @default.
• W2772476487 hasRelatedWork W2082020414 @default.
• W2772476487 hasRelatedWork W2189378924 @default.
• W2772476487 hasRelatedWork W2396519212 @default.
• W2772476487 hasRelatedWork W2765773067 @default.
• W2772476487 hasRelatedWork W2772476487 @default.
• W2772476487 hasRelatedWork W2891908181 @default.
• W2772476487 hasRelatedWork W204514590 @default.
• W2772476487 hasRelatedWork W2518053387 @default.
• W2772476487 hasVolume "33" @default.
• W2772476487 isParatext "false" @default.
• W2772476487 isRetracted "false" @default.
• W2772476487 magId "2772476487" @default.

• next