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dc.contributor.authorKanogwun Thongchoteen_US
dc.contributor.authorSaovaros Svastien_US
dc.contributor.authorMayurachat Sa-Ardriten_US
dc.contributor.authorNateetip Krishnamraen_US
dc.contributor.authorSuthat Fucharoenen_US
dc.contributor.authorNarattaphol Charoenphandhuen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-05-03T08:01:43Z-
dc.date.available2018-05-03T08:01:43Z-
dc.date.issued2011-07-01en_US
dc.identifier.citationHistochemistry and Cell Biology. Vol.136, No.1 (2011), 47-56en_US
dc.identifier.issn1432119Xen_US
dc.identifier.issn09486143en_US
dc.identifier.other2-s2.0-79960247513en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79960247513&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/11517-
dc.description.abstractβ-thalassemia caused by the C→T mutation at nucleotide 654 of the intron 2 (β IVSII-654 ) results in aberrant splicing of β-globin RNA, leading to an almost absence of β-globin synthesis. Although trabecular and cortical bone loss was previously reported in β-thalassemic mice with deletion of β-globin gene, the microscopic changes in trabecular structure in β IVSII-654 thalassemic mice remained elusive. Here, we investigated the macroscopic and microscopic bone changes in 12-week-old β IVSII-654 knockin thalassemic mice by dual-energy X-ray absorptiometry (DXA) and histomorphometric analysis, respectively. DXA revealed a decrease in bone mineral density in the lumbar vertebrae and tibial metaphysis, but not in the femoral diaphysis, suggesting that β IVSII-654 thalassemia predominantly led to osteopenia at the trabecular site, but not the cortical site. Further histomorphometric analysis of the tibial secondary spongiosa showed that trabecular bone volume was significantly decreased with the expansion of marrow cavity. Decreases in osteoblast surface, osteoid surface, mineral apposition rate, mineralizing surface, and mineralized volume were also observed. Moreover, trabecular bone resorption was markedly enhanced as indicated by increases in the osteoclast surface and eroded surface. It could be concluded that β IVSII-654 thalassemia impaired bone formation and enhanced bone resorption, thereby leading to osteopenia especially at the trabecular sites, such as the tibial metaphysis. © 2011 Springer-Verlag.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79960247513&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectHealth Professionsen_US
dc.subjectMedicineen_US
dc.titleImpaired bone formation and osteopenia in heterozygous β<sup>iVSII-654</sup>knockin thalassemic miceen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1007/s00418-011-0823-1en_US
Appears in Collections:Scopus 2011-2015

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