| pubmed-article:10430604 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C0684336 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C0029418 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C0029453 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C1299583 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C1159978 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C1608386 | lld:lifeskim |
| pubmed-article:10430604 | lifeskim:mentions | umls-concept:C1549571 | lld:lifeskim |
| pubmed-article:10430604 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:10430604 | pubmed:dateCreated | 1999-8-17 | lld:pubmed |
| pubmed-article:10430604 | pubmed:abstractText | We recently identified a new gene, klotho, which is involved in the suppression of multiple aging phenotypes. The mouse homozygous for a disruption of the klotho locus (kl/kl) exhibited multiple pathological conditions resembling human aging. Histomorphometric analysis revealed low-turnover osteopenia in kl/kl mice. The decrease in bone formation exceeded that of bone resorption, resulting in a net bone loss. The number of osteoblast progenitors determined by ex vivo bone marrow cultures was reduced in kl/kl mice. In addition, cultured osteoblastic cells derived from kl/kl mice showed lower alkaline phosphatase activity and matrix nodule formation than those from wild-type mice. Osteoclastogenesis in the coculture of marrow cells and osteoblastic cells was decreased only when marrow cells originated from kl/kl mice independently of the origin of osteoblastic cells. We also found that the expression of osteoprotegerin, an osteoclastogenesis inhibitor, was significantly upregulated in kl/kl mice. We conclude that a defect in the klotho gene expression causes the independent impairment of both osteoblast and osteoclast differentiation, leading to low-turnover osteopenia. Because this state represents a characteristic feature of senile osteoporosis in humans, kl/kl mice can be regarded as a useful model for investigating cellular and molecular mechanisms of age-related bone loss. | lld:pubmed |
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| pubmed-article:10430604 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10430604 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10430604 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10430604 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10430604 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:10430604 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:10430604 | pubmed:author | pubmed-author:ManabeNN | lld:pubmed |
| pubmed-article:10430604 | pubmed:author | pubmed-author:NakamuraKK | lld:pubmed |
| pubmed-article:10430604 | pubmed:author | pubmed-author:KawaguchiHH | lld:pubmed |
| pubmed-article:10430604 | pubmed:author | pubmed-author:MiyauraCC | lld:pubmed |
| pubmed-article:10430604 | pubmed:author | pubmed-author:Kuro-oMM | lld:pubmed |
| pubmed-article:10430604 | pubmed:author | pubmed-author:ChikudaHH | lld:pubmed |
| pubmed-article:10430604 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10430604 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:10430604 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10430604 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10430604 | pubmed:pagination | 229-37 | lld:pubmed |
| pubmed-article:10430604 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10430604 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10430604 | pubmed:articleTitle | Independent impairment of osteoblast and osteoclast differentiation in klotho mouse exhibiting low-turnover osteopenia. | lld:pubmed |
| pubmed-article:10430604 | pubmed:affiliation | Department of Orthopaedic Surgery, Faculty of Medicine, University of Tokyo, Tokyo 113-8655, Japan. kawaguchi-ort@h.u-tokyo.edu | lld:pubmed |
| pubmed-article:10430604 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10430604 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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