Linked Life Data

9299545

Source:http://linkedlifedata.com/resource/pubmed/id/9299545

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-10-16
pubmed:databankReference
pubmed:abstractText
Osteoblast stimulating factor-1 (OSF-1) stimulates in vitro proliferation and differentiation of osteoblastic cells, and its gene is expressed in the bone and brain tissues in mammals and amphibians. To evaluate the in vivo function of OSF-1 in bone metabolism, transgenic mice overexpressing the human osf-1 gene driven by the osteocalcin promoter were generated. Femoral bone mineral content was increased in transgenic mice relative to wild-type controls as estimated by ash assay, depending on the transgene copy number per cell. In ovariectomized mice, bone mass loss due to estrogen deficiency was observed in both transgenic and control mice but bone mass was still higher in transgenic mice than in controls. Bone mass in ovariectomized transgenic mice was comparable to that in wild-type mice without ovariectomy. These observations indicate that OSF-1 may direct in vivo appositional bone formation by increasing osteoblast activity rather than decreasing osteoclast activity, suggesting a new way to treat osteoporosis with OSF-1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 1997 Academic Press.
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
238
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
528-33
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Bone mass loss due to estrogen deficiency is compensated in transgenic mice overexpressing human osteoblast stimulating factor-1.
pubmed:affiliation
Research Institute for Neurological Diseases and Geriatrics, Second Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kamigyo-Ku, Kyoto, 602, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't