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Over-expression of Adamts1 in mice alters bone mineral density
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakogenomik och osteoporos.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
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2012 (Engelska)Ingår i: Journal of Bone and Mineral Metabolism, ISSN 0914-8779, E-ISSN 1435-5604, Vol. 30, nr 3, s. 304-311Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

ADAMTS1, a secreted multifunctional metalloproteinase with disintegrin and thrombospondin motifs, is an early response gene of parathyroid hormone (PTH) in osteoblasts. Mice engineered to lack Adamts1 are smaller compared to wild-type (WT) mice and ADAMTS1 metalloproteinase activity has been shown to increase osteoblastic growth in collagen gels. However, there are no reports investigating the consequence of Adamts1 over-expression on bone tissue in vivo. Here, we analyze bones of female and male transgenic (TG) mice over-expressing mouse Adamts1 using peripheral quantitative computed tomography to evaluate its effect on bone shape and mineral density. Western blotting of protein extracts and immunohistochemistry of bone sections reveal increased presence of Adamts1 protein in TG bones compared to WT bones. Phenotypic analyses of femur show that female TG mice have reduced metaphyseal total density, trabecular bone mineral density and trabecular mineral content. In contrast, male TG mice which were without changes in the metaphysis showed increased total density and cortical density at the mid-diaphysis cortical site. Female TG mice showed no significant changes at the cortical site compared to WT mice. Furthermore, diaphyseal endosteal compartment was only affected in male TG mice. Along these lines, Adamts1 increased blood levels of PTH only in females whereas it reduced osteocalcin levels only in males. These results reveal that Adamts1 has an impact on bone mineral density and thus further confirm Adamts1 as a potent regulator of bone remodeling.

Ort, förlag, år, upplaga, sidor
2012. Vol. 30, nr 3, s. 304-311
Nationell ämneskategori
Medicin och hälsovetenskap
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URN: urn:nbn:se:uu:diva-165560DOI: 10.1007/s00774-011-0322-4ISI: 000304825300005PubMedID: 22002813OAI: oai:DiVA.org:uu-165560DiVA, id: diva2:474259
Tillgänglig från: 2012-01-09 Skapad: 2012-01-09 Senast uppdaterad: 2017-12-08Bibliografiskt granskad

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Jonsson, Kenneth BMelhus, HåkanLind, Thomas

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