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Article: Sodium/myo-inositol cotransporter 1 and myo-inositol are essential for osteogenesis and bone formation

TitleSodium/myo-inositol cotransporter 1 and myo-inositol are essential for osteogenesis and bone formation
Authors
Keywordsbone formation
myo-inositol
osteogenesis
Smit1
Issue Date2011
PublisherAmerican Society for Bone and Mineral Research. The Journal's web site is located at http://www.jbmr.org/view/0/index.html
Citation
Journal Of Bone And Mineral Research, 2011, v. 26 n. 3, p. 582-590 How to Cite?
Abstract
myo-Inositol (MI) plays an essential role in several important processes of cell physiology, is involved in the neural system, and provides an effective treatment for some psychiatric disorders. Its role in osteogenesis and bone formation nonetheless is unclear. Sodium/MI cotransporter 1 (SMIT1, the major cotransporter of MI) knockout (SMIT1 -/-) mice with markedly reduced tissue MI levels were used to characterize the essential roles of MI and SMIT1 in osteogenesis. SMIT1 -/- embryos had a dramatic delay in prenatal mineralization and died soon after birth owing to respiratory failure, but this could be rescued by maternal MI supplementation. The rescued SMIT1 -/- mice had shorter limbs, decreased bone density, and abnormal bone architecture in adulthood. Deletion of SMIT1 resulted in retarded postnatal osteoblastic differentiation and bone formation in vivo and in vitro. Continuous MI supplementation partially restored the abnormal bone phenotypes in adult SMIT1 -/- mice and strengthened bone structure in SMIT1 +/+ mice. Although MI content was much lower in SMIT1 -/- mesenchymal cells (MSCs), the I(1,4,5)P 3 signaling pathway was excluded as the means by which SMIT1 and MI affected osteogenesis. PCR expression array revealed Fgf4, leptin, Sele, Selp, and Nos2 as novel target genes of SMIT1 and MI. SMIT1 was constitutively expressed in multipotential C3H10T1/2 and preosteoblastic MC3T3-E1 cells and could be upregulated during bone morphogenetic protein 2 (BMP-2)-induced osteogenesis. Collectively, this study demonstrated that deficiency in SMIT1 and MI has a detrimental impact on prenatal skeletal development and postnatal bone remodeling and confirmed their essential roles in osteogenesis, bone formation, and bone mineral density (BMD) determination. © 2011 American Society for Bone and Mineral Research. Copyright © 2011 American Society for Bone and Mineral Research.
Persistent Identifierhttp://hdl.handle.net/10722/133316
ISSN
2013 Impact Factor: 6.589
ISI Accession Number ID
Funding AgencyGrant Number
KC Wong Education Foundation
Osteoporosis and Endocrine Research, the University of Hong Kong
Funding Information:

ZD was supported by the KC Wong Education Foundation. This project was supported by the Osteoporosis and Endocrine Research, the University of Hong Kong.

References

 

Author Affiliations
  1. The University of Hong Kong
  2. Nanjing Medical University
DC FieldValueLanguage
dc.contributor.authorDai, Zen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorMiao, Den_HK
dc.contributor.authorLau, KSen_HK
dc.contributor.authorChan, AWHen_HK
dc.contributor.authorKung, AWCen_HK
dc.date.accessioned2011-05-11T08:30:38Z-
dc.date.available2011-05-11T08:30:38Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Bone And Mineral Research, 2011, v. 26 n. 3, p. 582-590en_HK
dc.identifier.issn0884-0431en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133316-
dc.description.abstractmyo-Inositol (MI) plays an essential role in several important processes of cell physiology, is involved in the neural system, and provides an effective treatment for some psychiatric disorders. Its role in osteogenesis and bone formation nonetheless is unclear. Sodium/MI cotransporter 1 (SMIT1, the major cotransporter of MI) knockout (SMIT1 -/-) mice with markedly reduced tissue MI levels were used to characterize the essential roles of MI and SMIT1 in osteogenesis. SMIT1 -/- embryos had a dramatic delay in prenatal mineralization and died soon after birth owing to respiratory failure, but this could be rescued by maternal MI supplementation. The rescued SMIT1 -/- mice had shorter limbs, decreased bone density, and abnormal bone architecture in adulthood. Deletion of SMIT1 resulted in retarded postnatal osteoblastic differentiation and bone formation in vivo and in vitro. Continuous MI supplementation partially restored the abnormal bone phenotypes in adult SMIT1 -/- mice and strengthened bone structure in SMIT1 +/+ mice. Although MI content was much lower in SMIT1 -/- mesenchymal cells (MSCs), the I(1,4,5)P 3 signaling pathway was excluded as the means by which SMIT1 and MI affected osteogenesis. PCR expression array revealed Fgf4, leptin, Sele, Selp, and Nos2 as novel target genes of SMIT1 and MI. SMIT1 was constitutively expressed in multipotential C3H10T1/2 and preosteoblastic MC3T3-E1 cells and could be upregulated during bone morphogenetic protein 2 (BMP-2)-induced osteogenesis. Collectively, this study demonstrated that deficiency in SMIT1 and MI has a detrimental impact on prenatal skeletal development and postnatal bone remodeling and confirmed their essential roles in osteogenesis, bone formation, and bone mineral density (BMD) determination. © 2011 American Society for Bone and Mineral Research. Copyright © 2011 American Society for Bone and Mineral Research.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Bone and Mineral Research. The Journal's web site is located at http://www.jbmr.org/view/0/index.htmlen_HK
dc.relation.ispartofJournal of Bone and Mineral Researchen_HK
dc.subjectbone formationen_HK
dc.subjectmyo-inositolen_HK
dc.subjectosteogenesisen_HK
dc.subjectSmit1en_HK
dc.subject.meshAging - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBone and Bones - embryology - pathologyen_HK
dc.subject.meshCell Counten_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshEmbryo, Mammalian - metabolismen_HK
dc.subject.meshGene Deletionen_HK
dc.subject.meshInositol - metabolismen_HK
dc.subject.meshInositol 1,4,5-Trisphosphate - metabolismen_HK
dc.subject.meshIntracellular Space - metabolismen_HK
dc.subject.meshMesenchymal Stem Cells - cytology - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshOrgan Sizeen_HK
dc.subject.meshOsteoblasts - metabolism - pathologyen_HK
dc.subject.meshOsteogenesisen_HK
dc.subject.meshOsteoporosis - metabolism - pathologyen_HK
dc.subject.meshSymporters - deficiency - metabolismen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.titleSodium/myo-inositol cotransporter 1 and myo-inositol are essential for osteogenesis and bone formationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0884-0431&volume=26&issue=3&spage=582&epage=590&date=2011&atitle=Sodium/+myo+‐inositol+cotransporter+1+and+myo+‐inositol+are+essential+for+osteogenesis+and+bone+formation-
dc.identifier.emailChung, SK:skchung@hkucc.hku.hken_HK
dc.identifier.emailKung, AWC:awckung@hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityKung, AWC=rp00368en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jbmr.240en_HK
dc.identifier.pmid20818642en_HK
dc.identifier.scopuseid_2-s2.0-79951842355en_HK
dc.identifier.hkuros184858en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79951842355&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue3en_HK
dc.identifier.spage582en_HK
dc.identifier.epage590en_HK
dc.identifier.isiWOS:000287827600019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDai, Z=39560959900en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridMiao, D=7006323446en_HK
dc.identifier.scopusauthoridLau, KS=35205833900en_HK
dc.identifier.scopusauthoridChan, AWH=37019615700en_HK
dc.identifier.scopusauthoridKung, AWC=7102322339en_HK

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