FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1480595589> ?p ?o ?g. }

• W1480595589 endingPage "1459" @default.
• W1480595589 startingPage "1451" @default.
• W1480595589 abstract "Abstract We investigated the mechanisms of sickle cell disease (SCD) hematopoietic/erythropoietic defects using bone marrow, spleen, and/or peripheral blood from the transgenic SAD mouse model, which closely reproduces the biochemical and physiological disorders observed in human SCD. First, the erythropoietic lineage late precursors (polychromatophilic normoblasts to the intramedullary reticulocytes) of SAD mouse bone marrow were significantly altered morphologically. These anomalies resulted from high levels of hemoglobin polymers and were associated with increased cell fragmentation occurring during medullary endothelial migration of reticulocytes. Secondly, analysis of bone marrow erythropoiesis in earlier stages showed a marked depletion in SAD erythroid burst-forming units (BFU-E; of ∼42%) and erythroid colony-forming units (CFU-E; of ∼23%) progenitors, despite a significant increase in their proliferation, suggesting a compensatory mechanism. In contrast to the bone marrow progenitor depletion, we observed (1) a high mobilization/relocation of BFU-E early progenitors (∼4-fold increase) in peripheral blood of SAD mice as well as of colony-forming units–granulocyte-macrophage (CFU-GM) and (2) a 7-fold increase of SAD CFU-E in the spleen. Third, and most importantly, SAD bone marrow multipotent cells (spleen colony-forming units [CFU-S], granulocyte-erythroid-macrophage-megakaryocyte colony-forming units [CFU-GEMM], and Sca+Lin−) were highly mobilized to the peripheral blood (∼4-fold increase), suggesting that peripheral multipotent cells could serve as proliferative and autologous vehicles for gene therapy. Therefore, we conclude the following. (1) The abnormal differentiation and morphology of late nucleated erythroid precursors result in an ineffective sickle erythropoiesis and likely contribute to the pathophysiology of sickle cell disorders; this suggests that transfer of normal or modified SCD bone marrow cells may have a selective advantage in vivo. (2) A hematopoietic compensatory mechanism exists in SAD/SCD pathology and consists of mobilization of multipotent cells from the bone marrow to the peripheral blood and their subsequent uptake into the spleen, an extramedullary hematopoietic site for immediate differentiation. Altogether, these results corroborate the strong potential effectiveness of both autologous and allogeneic bone marrow transplantation for SCD hematopoietic therapy." @default.
• W1480595589 created "2016-06-24" @default.
• W1480595589 creator A5011764402 @default.
• W1480595589 creator A5021097392 @default.
• W1480595589 creator A5061545003 @default.
• W1480595589 date "1999-08-15" @default.
• W1480595589 modified "2023-10-17" @default.
• W1480595589 title "Altered Hematopoiesis in Murine Sickle Cell Disease" @default.
• W1480595589 cites W1666010738 @default.
• W1480595589 cites W173907651 @default.
• W1480595589 cites W1951306441 @default.
• W1480595589 cites W1965423787 @default.
• W1480595589 cites W1965455211 @default.
• W1480595589 cites W1972406498 @default.
• W1480595589 cites W1975450626 @default.
• W1480595589 cites W1977708103 @default.
• W1480595589 cites W1989971434 @default.
• W1480595589 cites W2002487300 @default.
• W1480595589 cites W2005821035 @default.
• W1480595589 cites W2024079226 @default.
• W1480595589 cites W2034718815 @default.
• W1480595589 cites W2038898665 @default.
• W1480595589 cites W2041211702 @default.
• W1480595589 cites W2054668591 @default.
• W1480595589 cites W2069854753 @default.
• W1480595589 cites W2076347749 @default.
• W1480595589 cites W2088391010 @default.
• W1480595589 cites W2115503586 @default.
• W1480595589 cites W2140988398 @default.
• W1480595589 cites W2152317092 @default.
• W1480595589 cites W2262928512 @default.
• W1480595589 cites W2324143840 @default.
• W1480595589 cites W2395895968 @default.
• W1480595589 cites W2409000741 @default.
• W1480595589 cites W2786344329 @default.
• W1480595589 cites W59086279 @default.
• W1480595589 cites W75372324 @default.
• W1480595589 cites W92205045 @default.
• W1480595589 doi "https://doi.org/10.1182/blood.v94.4.1451" @default.
• W1480595589 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10438733" @default.
• W1480595589 hasPublicationYear "1999" @default.
• W1480595589 type Work @default.
• W1480595589 sameAs 1480595589 @default.
• W1480595589 citedByCount "31" @default.
• W1480595589 countsByYear W14805955892014 @default.
• W1480595589 countsByYear W14805955892015 @default.
• W1480595589 countsByYear W14805955892016 @default.
• W1480595589 countsByYear W14805955892017 @default.
• W1480595589 countsByYear W14805955892018 @default.
• W1480595589 countsByYear W14805955892020 @default.
• W1480595589 countsByYear W14805955892021 @default.
• W1480595589 countsByYear W14805955892022 @default.
• W1480595589 crossrefType "journal-article" @default.
• W1480595589 hasAuthorship W1480595589A5011764402 @default.
• W1480595589 hasAuthorship W1480595589A5021097392 @default.
• W1480595589 hasAuthorship W1480595589A5061545003 @default.
• W1480595589 hasConcept C109159458 @default.
• W1480595589 hasConcept C126322002 @default.
• W1480595589 hasConcept C201750760 @default.
• W1480595589 hasConcept C203014093 @default.
• W1480595589 hasConcept C2778248108 @default.
• W1480595589 hasConcept C2779703530 @default.
• W1480595589 hasConcept C2779705218 @default.
• W1480595589 hasConcept C2779813244 @default.
• W1480595589 hasConcept C2780007613 @default.
• W1480595589 hasConcept C2780844101 @default.
• W1480595589 hasConcept C2780931953 @default.
• W1480595589 hasConcept C28328180 @default.
• W1480595589 hasConcept C71924100 @default.
• W1480595589 hasConcept C86803240 @default.
• W1480595589 hasConcept C95444343 @default.
• W1480595589 hasConcept C95862172 @default.
• W1480595589 hasConceptScore W1480595589C109159458 @default.
• W1480595589 hasConceptScore W1480595589C126322002 @default.
• W1480595589 hasConceptScore W1480595589C201750760 @default.
• W1480595589 hasConceptScore W1480595589C203014093 @default.
• W1480595589 hasConceptScore W1480595589C2778248108 @default.
• W1480595589 hasConceptScore W1480595589C2779703530 @default.
• W1480595589 hasConceptScore W1480595589C2779705218 @default.
• W1480595589 hasConceptScore W1480595589C2779813244 @default.
• W1480595589 hasConceptScore W1480595589C2780007613 @default.
• W1480595589 hasConceptScore W1480595589C2780844101 @default.
• W1480595589 hasConceptScore W1480595589C2780931953 @default.
• W1480595589 hasConceptScore W1480595589C28328180 @default.
• W1480595589 hasConceptScore W1480595589C71924100 @default.
• W1480595589 hasConceptScore W1480595589C86803240 @default.
• W1480595589 hasConceptScore W1480595589C95444343 @default.
• W1480595589 hasConceptScore W1480595589C95862172 @default.
• W1480595589 hasIssue "4" @default.
• W1480595589 hasLocation W14805955891 @default.
• W1480595589 hasOpenAccess W1480595589 @default.
• W1480595589 hasPrimaryLocation W14805955891 @default.
• W1480595589 hasRelatedWork W1975791409 @default.
• W1480595589 hasRelatedWork W1989415625 @default.
• W1480595589 hasRelatedWork W2018903526 @default.
• W1480595589 hasRelatedWork W2134304007 @default.
• W1480595589 hasRelatedWork W2414720610 @default.
• W1480595589 hasRelatedWork W2417320181 @default.

• next