About: Apolipoprotein D deficiency is associated to high bone turnover, low bone mass and impaired osteoblastic function in aged female mice

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About: Apolipoprotein D deficiency is associated to high bone turnover, low bone mass and impaired osteoblastic function in aged female mice Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Apolipoprotein D deficiency is associated to high bone turnover, low bone mass and impaired osteoblastic function in aged female mice
Creator	Najyb, Ouafa Martineau, Corine Moreau, Robert Rassart, Éric Signor, Céline
Source	Elsevier; Medline; PMC
abstract	Abstract Background Apolipoprotein D (ApoD) is a member of the lipocalin family known to transport small hydrophobic ligands. A major site of ApoD expression in mice is the central nervous system where evidence suggests that it plays a protective role. Gene expression of ApoD was reported in bone-forming osteoblasts but its impact on bone metabolism remains undocumented. Methods We compared basic bone parameters of ApoD −/− (null) and transgenic (tg) mice to wild-type (wt) littermates through microCT and histochemistry, as well as ApoD expression and secretion in osteoblasts under various culture conditions through real-time PCR and immunoblotting. Results ApoD-null females displayed progressive bone loss with aging, resulting in a 50% reduction in trabecular bone volume and a 23% reduction in cortical bone volume by 9months of age. Only cortical bone volume was significantly reduced in ApoD-null males by an average of 24%. Histochemistry indicated significantly higher osteoblast surface and number of osteoclasts in femora from ApoD-null females. ApoD gene expression was confirmed in primary cultures of bone marrow mesenchymal cells (MSC), with higher expression levels in MSC from females compared to males. ApoD-null MSC exhibited impaired proliferation and differentiation potentials. Moreover, exogenous ApoD partially rescued the osteogenic potential of null MSC, which were shown to readily uptake the protein from media. ApoD expression was upregulated under low proliferation conditions, by contact inhibition and osteoblastic differentiation in MC3T3-E1 osteoblast-like cells. Conclusion Our results indicate that ApoD influences bone metabolism in mice in a gender-specific manner, potentially through an auto-/paracrine pathway.
has issue date	2016-09-30(xsd:dateTime)
bibo:doi	10.1016/j.metabol.2016.05.007
bibo:pmid	27506732
has license	els-covid
sha1sum (hex)	980fab09f09736ecdcae23f598486d65025efdba
schema:url	https://doi.org/10.1016/j.metabol.2016.05.007
resource representing a document's title	Apolipoprotein D deficiency is associated to high bone turnover, low bone mass and impaired osteoblastic function in aged female mice
has PubMed Central identifier	PMC7094319
has PubMed identifier	27506732
schema:publication	Metabolism
resource representing a document's body	covid:980fab09f09736ecdcae23f598486d65025efdba#body_text
is schema:about of	covid:arg/980fab09f09736ecdcae23f598486d65025efdba named entity 'member' named entity 'bone metabolism' named entity 'lipocalin' named entity 'remains' named entity 'ApoD' named entity 'ApoD' named entity 'Sarstedt' named entity 'ApoD' named entity 'trabeculae' named entity 'mice' named entity 'Ontario' named entity 'ApoD' named entity 'ApoD' named entity 'protein' named entity 'pyrimidine' named entity 'nervous tissue' named entity 'metaphysis' named entity 'high affinity' named entity 'G2/M' named entity 'phenotype' named entity 'age-related' named entity 'ApoD' named entity 'growth plate' named entity 'glycerol' named entity 'monocyte' named entity 'arachidonic acid' named entity 'biotechnology' named entity 'lipid peroxidation' named entity 'TRAP-positive' named entity 'ApoD' named entity 'MSC' named entity 'cancer cell lines' named entity 'ApoD' named entity 'lipid' named entity 'osteogenic' named entity 'Opg' named entity 'penicillin' named entity 'ApoD' named entity 'osteoblast' named entity 'murine' named entity 'triton X-100' named entity 'mRNA' named entity 'G1 phase' named entity 'bone metabolism' named entity 'Plasma' named entity 'upregulation' named entity 'Invitrogen' named entity 'polymethylmethacrylate' named entity 'mice' named entity 'bone tissue' named entity 'protein' named entity 'Canada' named entity 'gene' named entity 'osteogenic' named entity 'Canadian Institutes of Health Research' named entity 'starvation' named entity 'null mice' named entity 'Invitrogen' named entity 'ApoD' named entity 'microtiter' named entity 'organism' named entity 'ApoD' named entity 'ApoD' named entity 'osteoblasts' named entity 'Canada' named entity 'MSC' named entity 'Femora' named entity 'tibiae' named entity 'osteoblasts' named entity 'MSC' named entity 'progesterone' named entity 'human coronavirus OC43' named entity 'Bio-Rad' named entity 'PCR' named entity 'mouse strains' named entity 'mice'

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