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  • 1
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    Estrogen Receptor β ( ESR2 ) Polymorphisms in Interaction With Estrogen Receptor α ( ESR1) and Insulin‐Like Growth Factor I ( IGF1 ) Variants Influence the Risk of Fracture in Postmenopausal Women
    Wiley ; 2006
    In:  Journal of Bone and Mineral Research Vol. 21, No. 9 ( 2006-09), p. 1443-1456
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 21, No. 9 ( 2006-09), p. 1443-1456
    Abstract: In this large population‐based cohort study, variants in ESR2 were associated with increased risk of vertebral and incident fragility fracture in postmenopausal women. Interaction of ESR2 with ESR1 and IGF1 was determined and revealed a deleterious genetic combination that enhances the risk of osteoporotic fracture. Introduction: Osteoporosis is a complex disease with strong genetic influence, but the genes involved are ill‐defined. We examined estrogen receptor β ( ESR2) polymorphisms in interaction with estrogen receptor α ( ESR1) and insulin‐like growth factor I ( IGF1) variants in relation to the risk of osteoporotic fracture, BMD, and bone geometry. Materials and Methods: In the Rotterdam study, a prospective population‐based cohort of elderly white individuals, we studied six single nucleotide polymorphisms (SNPs) in ESR2 ( n = 6343, 60% women). We analyzed the genetic variants in the form of haplotypes reconstructed by a statistical method. Results refer to the most frequent ESR2 haplotype 1 estimated from two SNPs in intron 2 and the 3′‐untranslated region (UTR). Outcomes included vertebral and incident nonvertebral fractures, BMD, and hip structural analysis (HSA). We also studied the interaction with (the most frequent) ESR1 haplotype 1 estimated from the Pvu II and Xba I polymorphisms and an IGF1 promoter CA‐repeat. Results: Compared with ESR2 haplotype 1 noncarriers, female homozygous carriers had a 1.8‐ and 1.4‐fold increased risk of vertebral and fragility fractures. HSA showed that ESR2 haplotype 1 homozygote women had 2.6% thinner cortices, 1.0% increased neck width, and 4.3% higher bone instability (buckling ratios). For testing the gene interaction, we assumed a recessive model of ESR2 haplotype 1 . Female homozygous carriers of ESR2 haplotype 1 and noncarriers of ESR1 haplotype 1 had a 3.5‐ and 1.8‐fold increased risk of vertebral and fragility fractures ( p interaction = 0.10). Such effects and interactions were stronger in women homozygous for the IGF1 192‐bp allele, with 9.3‐fold increased risk ( p interaction = 0.002) for vertebral and 4.0‐fold increased risk ( p interaction = 0.01) for fragility fractures. Multilocus interaction analyses of fracture endured correction for multiple testing using Monte‐Carlo simulations ( p interaction = 0.02 for vertebral and p interaction = 0.03 for fragility fractures). Similar patterns of interaction were observed for BMD, cortical thickness, bone strength (section modulus), and instability (buckling ratio). In men, no such effects were observed. Conclusions: Variants of ESR2 alone and in interaction with ESR1 and IGF1 influence the risk of fracture in postmenopausal women. These findings reinforce the polygenic and complex character of osteoporosis.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Article
    DOI: 10.1359/jbmr.060605
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2006
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  • 2
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    Identification of Chloride Intracellular Channel Protein 3 as a Novel Gene Affecting Human Bone Formation
    Wiley ; 2017
    In:  JBMR Plus Vol. 1, No. 1 ( 2017-08), p. 16-26
    Details
    In: JBMR Plus, Wiley, Vol. 1, No. 1 ( 2017-08), p. 16-26
    Abstract: Osteoporosis is a common skeletal disorder characterized by low bone mass leading to increased bone fragility and fracture susceptibility. The bone building cells, osteoblasts, are derived from mesenchymal stromal cells (MSCs); however, with increasing age osteogenic differentiation is diminished and more adipocytes are seen in the bone marrow, suggesting a shift in MSC lineage commitment. Identification of specific factors that stimulate osteoblast differentiation from human MSCs may deliver therapeutic targets to treat osteoporosis. The aim of this study was to identify novel genes involved in osteoblast differentiation of human bone marrow–derived MSCs (hMSCs). We identified the gene chloride intracellular channel protein 3 ( CLIC3 ) to be strongly upregulated during MSC‐derived osteoblast differentiation. Lentiviral overexpression of CLIC3 in hMSCs caused a 60% increase of matrix mineralization. Conversely, knockdown of CLIC3 in hMSCs using two short‐hairpin RNAs (shRNAs) against CLIC3 resulted in a 69% to 76% reduction in CLIC3 mRNA expression, 53% to 37% less alkaline phosphatase (ALP) activity, and 78% to 88% less matrix mineralization compared to scrambled control. Next, we used an in vivo human bone formation model in which hMSCs lentivirally transduced with the CLIC3 overexpression construct were loaded onto a scaffold (hydroxyapatite‐tricalcium‐phosphate), implanted under the skin of NOD‐SCID mice, and analyzed for bone formation 8 weeks later. CLIC3 overexpression led to a 15‐fold increase in bone formation (0.33% versus 5.05% bone area relative to scaffold). Using a Clic3‐His‐tagged pull‐down assay and liquid chromatography–mass spectrometry (LS/MS)‐based proteomics analysis in lysates of osteogenically differentiated hMSCs, we showed that CLIC3 interacts with NIMA‐related kinase 9 (NEK9) and phosphatidylserine synthase 1 (PTDSS1) in vitro, and this finding was supported by immunofluorescent analysis. In addition, inhibition of NEK9 or PTDSS1 gene expression by shRNAs inhibited osteoblast differentiation and mineralization. In conclusion, we successfully identified CLIC3 to be a lineage‐specific gene regulating osteoblast differentiation and bone formation through its interaction with NEK9 and PTDSS1. © The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
    Type of Medium: Online Resource
    ISSN: 2473-4039 , 2473-4039
    URL: Issue
    URL: Article
    DOI: 10.1002/jbm4.v1.1
    DOI: 10.1002/jbm4.10003
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2905710-3
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  • 3
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    Better knowledge on vitamin D and calcium in older people is associated with a higher serum vitamin D level and a higher daily dietary calcium intake
    SAGE Publications ; 2012
    In:  Health Education Journal Vol. 71, No. 4 ( 2012-07), p. 474-482
    Details
    In: Health Education Journal, SAGE Publications, Vol. 71, No. 4 ( 2012-07), p. 474-482
    Abstract: Objective: The objective of the present study was to examine knowledge on vitamin D and calcium in a cohort of older adults and to test the association between health knowledge, vitamin D status and dietary calcium intake. Methods: The participants of this cross-sectional survey consisted of 426 individuals (≥65 years), living in residential homes. Participants were tested for their knowledge on vitamin D and calcium using a standardized questionnaire. Serum 25-hydroxyvitamin D 3 (25(OH)D 3 ) levels and dietary calcium intake were measured. Results: The mean serum 25(OH)D 3 level was 39.1 (±21.4) nmol/l and the mean daily dietary calcium intake was 826 (±242) mg/day. Of the participants, only 38 per cent indicated that they knew or had heard of vitamin D. Participants overestimated their daily calcium intake. Better knowledge on vitamin D and calcium was associated with both higher vitamin D levels ( P 〈 0.0001) and a higher daily dietary calcium intake ( P 〈 0.0001). Conclusion: Given the poor knowledge on vitamin D and calcium and the observed associations, improving health knowledge could be a possible intervention to improve vitamin D status and calcium intake in older people. Further studies are needed to assess whether education will indeed lead to improvement of vitamin D levels and calcium intake in this age group.
    Type of Medium: Online Resource
    ISSN: 0017-8969 , 1748-8176
    URL: Article
    DOI: 10.1177/0017896911406965
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
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  • 4
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    Mucin 1 (Muc1) Deficiency in Female Mice Leads to Temporal Skeletal Changes During Aging
    Wiley ; 2018
    In:  JBMR Plus Vol. 2, No. 6 ( 2018-11), p. 341-350
    Details
    In: JBMR Plus, Wiley, Vol. 2, No. 6 ( 2018-11), p. 341-350
    Abstract: Mucin1 (MUC1) encodes a glycoprotein that has been demonstrated to have important roles in cell‐cell interactions, cell‐matrix interactions, cell signaling, modulating tumor progression and metastasis, and providing physical protection to cells against pathogens. In this study, we investigated the bone phenotype in female C57BL/6 Muc1 null mice and the impact of the loss of Muc1 on osteoblasts and osteoclasts. We found that deletion of Muc1 results in reduced trabecular bone volume in 8‐week‐old mice compared with wild‐type controls, but the trabecular bone volume fraction normalizes with increasing age. In mature female mice (16 weeks old), Muc1 deletion results in stiffer femoral bones with fewer osteoblasts lining the trabecular surface but increased endosteal mineralized surface and bone formation rate. The latter remains higher compared with wild‐type females at age 52 weeks. No difference was found in osteoclast numbers in vivo and in bone marrow osteoblast or osteoclast differentiation capacity or activity in vitro. Taken together, these results suggest that Muc1 depletion causes a transiently reduced trabecular bone mass phenotype in young mice, and later in life reduced numbers of osteoblasts with increased endocortical mineralization activity coincides with unaffected total bone mass and increased stiffness. In conclusion, our results show, for the first time to our knowledge, a role for Muc1 in bone mass and mineralization in mice in a time‐dependent manner. © 2018 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
    Type of Medium: Online Resource
    ISSN: 2473-4039 , 2473-4039
    URL: Issue
    URL: Article
    DOI: 10.1002/jbm4.v2.6
    DOI: 10.1002/jbm4.10061
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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  • 5
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    Cdx‐2 Polymorphism in the Promoter Region of the Human Vitamin D Receptor Gene Determines Susceptibility to Fracture in the Elderly
    Wiley ; 2003
    In:  Journal of Bone and Mineral Research Vol. 18, No. 9 ( 2003-09), p. 1632-1641
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 18, No. 9 ( 2003-09), p. 1632-1641
    Abstract: A Cdx‐2 binding site polymorphism (G to A) in the promoter region of the human vitamin D receptor gene was reported. In an ecological study in eight ethnic groups and an association study in 2848 elderly whites, we found the A ‐allele to be associated with decreased fracture risk. Our findings expand previous similar findings in a Japanese study to whites and show a relationship with fracture risk of this functional polymorphism. Introduction: A single nucleotide polymorphism (SNP) within a binding site of the intestinal‐specific transcription factor Cdx‐2 in the promoter region of the human vitamin D receptor ( VDR ) gene was previously reported. It was found to modulate the transcription of the hVDR gene and to be associated with decreased bone mineral density in a small group of postmenopausal Japanese women. In this study, we investigated the relationship between the VDR Cdx‐2 genotype and risk of fracture. Methods: We first determined the location of this SNP in the VDR gene by sequencing analysis, and we developed an allele‐specific multiplex polymerase chain reaction test to determine the Cdx‐2 genotype. We then performed an ecological study in eight ethnic groups and an association analysis in a large epidemiological cohort of 2848 Dutch white men and women, ≥55 years old. Results and Conclusions: The location of the G to A substitution was found in the promoter region of exon 1e (1e‐G−1739A) of the VDR gene. By comparing the frequency of the A ‐allele in eight different ethnic groups, we observed a negative correlation between prevalence of the A ‐allele and published hip fracture incidence rates in these ethnic groups ( p = 0.006 for men and p = 0.02 for women), suggesting a protective effect of this allele on fracture risk. Subsequently, in the association study, the A ‐allele (population frequency 19%) was observed to have a protective effect on occurrence of osteoporotic fractures, especially for nonvertebral fracture in women (relative risk of AA versus GG genotype is 0.2; 95% CI, 0.05–0.8). This effect remained after adjustment for age, weight, and bone mineral density. We conclude that the A ‐allele of the VDR Cdx‐2 polymorphism is present in whites, albeit at low frequency, and show a protective effect of this allele on risk of fracture.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Article
    DOI: 10.1359/jbmr.2003.18.9.1632
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2003
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  • 6
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    The T‐13910C polymorphism in the lactase phlorizin hydrolase gene is associated with differences in serum calcium levels and calcium intake
    Wiley ; 2010
    In:  Journal of Bone and Mineral Research Vol. 25, No. 9 ( 2010-09), p. 1980-1987
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 25, No. 9 ( 2010-09), p. 1980-1987
    Abstract: The C‐variant of a T‐13910C polymorphism (rs4988235; NT_022135.15:g.25316568G  〉  A) upstream of the lactase phlorizin hydrolase (LPH) gene causes lactose intolerance. Association studies with differences in bone parameters and fracture risk have been inconclusive. The objective of this study was to examine the association of LPH rs4988235 with body height and bone parameters and calcium homeostasis in two elderly populations of Dutch Caucasians and assess interaction with vitamin D receptor (VDR) polymorphisms. Genotyping of LPH and VDR polymorphisms was performed in 6367 individuals from the Rotterdam Study and 844 from the Longitudinal Aging Study Amsterdam (LASA). Associations with age, height, weight, bone mineral density (BMD), skeletal morphometric parameters and serum vitamin D and calcium levels, and dietary calcium intake were assessed using ANOVA or analysis of covariance, and allele dose effect was assessed using linear regression analysis. Fracture risk was analyzed using Cox's proportional hazard regression analysis. Associations with body height (p = 2.7 × 10 −8 ) and vertebral area (p = .048) found in the Rotterdam Study were explained by population stratification, as assessed by principal‐component analyses, and disappeared after additional adjustments. No associations with femoral neck or lumbar spine BMD or with fracture risk were detected. Calcium intake and serum ionized serum calcium were significantly lower in C‐homozygotes (p = 9.2 × 10 −7 , p = .02, respectively). For none of the parameters studied was interaction between the T‐13910C polymorphism and VDR block 5 haplotype 1 observed. We show that the C allele of the T‐13910C polymorphism causing lactose intolerance is associated with lower dietary calcium intake and serum calcium levels but not with BMD or fractures. The associations observed with height and vertebral area were the result of population stratification. This demonstrates the impact of population stratification and urges researchers to carefully take this into account in genetic associations, in particular, in dietary intake–related phenotypes, of which LPH and lactose intolerance are a strong example. © 2010 American Society for Bone and Mineral Research
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v25:9
    DOI: 10.1002/jbmr.83
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2010
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  • 7
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    A role for subchondral bone changes in the process of osteoarthritis; a micro-CT study of two canine models
    Springer Science and Business Media LLC ; 2008
    In:  BMC Musculoskeletal Disorders Vol. 9, No. 1 ( 2008-12)
    Details
    In: BMC Musculoskeletal Disorders, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2008-12)
    Abstract: This study evaluates changes in peri-articular bone in two canine models for osteoarthritis: the groove model and the anterior cruciate ligament transection (ACLT) model. Methods Evaluation was performed at 10 and 20 weeks post-surgery and in addition a 3-weeks time point was studied for the groove model. Cartilage was analysed, and architecture of the subchondral plate and trabecular bone of epiphyses was quantified using micro-CT. Results At 10 and 20 weeks cartilage histology and biochemistry demonstrated characteristic features of osteoarthritis in both models (very mild changes at 3 weeks). The groove model presented osteophytes only at 20 weeks, whereas the ACLT model showed osteophytes already at 10 weeks. Trabecular bone changes in the groove model were small and not consistent. This contrasts the ACLT model in which bone volume fraction was clearly reduced at 10 and 20 weeks (15–20%). However, changes in metaphyseal bone indicate unloading in the ACLT model, not in the groove model. For both models the subchondral plate thickness was strongly reduced (25–40%) and plate porosity was strongly increased (25–85%) at all time points studied. Conclusion These findings show differential regulation of subchondral trabecular bone in the groove and ACLT model, with mild changes in the groove model and more severe changes in the ACLT model. In the ACLT model, part of these changes may be explained by unloading of the treated leg. In contrast, subchondral plate thinning and increased porosity were very consistent in both models, independent of loading conditions, indicating that this thinning is an early response in the osteoarthritis process.
    Type of Medium: Online Resource
    ISSN: 1471-2474
    URL: Article
    DOI: 10.1186/1471-2474-9-20
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2008
    detail.hit.zdb_id: 2041355-5
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  • 8
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    Serum Phosphate Is Associated With Fracture Risk: The Rotterdam Study and MrOS
    Wiley ; 2017
    In:  Journal of Bone and Mineral Research Vol. 32, No. 6 ( 2017-06), p. 1182-1193
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 32, No. 6 ( 2017-06), p. 1182-1193
    Abstract: Extreme phosphate levels (P) have been associated with mineralization defects and increased fracture risk. Whether P within normal range is related to bone health in the general population is not well understood. To investigate the association of P with bone mineral density (BMD) and fracture risk, we assessed two population‐based cohorts: the Dutch Rotterdam Study (RS‐I, RS‐II, RS‐III; n  = 6791) and the US Osteoporotic Fractures in Men (MrOS; n  = 5425) study. The relationship of P with lumbar spine (LS) and femoral neck (FN) BMD was tested in all cohorts via linear models; fracture risk was tested in RS‐I, RS‐II, and MrOS through Cox models, after follow‐up of 8.6, 6.6, and 10.9 years, respectively. Adjustments were made for age, body mass index, smoking, serum levels of calcium, potassium, 25‐hydroxyvitamin D, estimated glomerular filtration rate (eGFR), FN‐BMD, prevalent diabetes, and cardiovascular disease. Additional adjustments were made for phosphate intake, parathyroid hormone, and fibroblast growth factor 23 levels in MrOS. We further stratified by eGFR. Results were pooled through study‐level meta‐analyses. Hazard ratios (HR) and betas (β) (from meta‐analyses) are expressed per 1 mg/dL P increase. P was positively associated with fracture risk in men and women from RS, and findings were replicated in MrOS (pooled HR all [95% CI]: 1.47 [1.31–1.65] ). P was associated with fracture risk in subjects without chronic kidney disease (CKD): all (1.44 [1.26–1.63]) and in men with CKD (1.93 [1.42–2.62] ). P was inversely related to LS‐BMD in men (β: –0.06 [–0.11 to –0.02]) and not to FN‐BMD in either sex. In summary, serum P was positively related to fracture risk independently from BMD and phosphate intake after adjustments for potential confounders. P and LS‐BMD were negatively related in men. Our findings suggest that increased P levels even within normal range might be deleterious for bone health in the normal population. © 2017 American Society for Bone and Mineral Research.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v32.6
    DOI: 10.1002/jbmr.3094
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2017
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  • 9
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    Understanding Age‐Induced Cortical Porosity in Women: The Accumulation and Coalescence of Eroded Cavities Upon Existing Intracortical Canals Is the Main Contributor
    Wiley ; 2018
    In:  Journal of Bone and Mineral Research Vol. 33, No. 4 ( 2018-04), p. 606-620
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 33, No. 4 ( 2018-04), p. 606-620
    Abstract: Intracortical bone remodeling normally ensures maintenance of the cortical bone matrix and strength, but during aging, this remodeling generates excessive porosity. The mechanism behind the age‐induced cortical porosity is poorly understood and addressed in the present study. This study consists of a histomorphometric analysis of sections of iliac bone specimens from 35 women (age 16–78 years). First, the study shows that the age‐induced cortical porosity reflects an increased pore size rather than an increased pore density. Second, it establishes a novel histomorphometric classification of the pores, which is based on the characteristics of the remodeling sites to which each pore is associated. It takes into consideration (i) the stage of the remodeling event at the level where the pore is sectioned, (ii) whether the event corresponds with the generation of a new pore through penetrative tunneling (type 1 pores) or with remodeling of an existing pore (type 2 pores), and (iii) in the latter case, whether or not the new remodeling event leads to the coalescence of pores. Of note, the advantage of this classification is to relate porosity with its generation mechanism. Third, it demonstrates that aging and porosity are correlated with: a shift from type 1 to type 2 pores, reflecting that the remodeling of existing pores is higher; an accumulation of eroded type 2 pores, reflecting an extended resorption‐reversal phase; and a coalescence of these eroded type 2 pores into enlarged coalescing type 2 cavities. Collectively, this study supports the notion, that age‐related increase in cortical porosity is the result of intracortical remodeling sites upon existing pores, with an extended reversal‐resorption phase (eroded type 2 pores) that may likely result in a delayed or absent initiation of the subsequent bone formation. © 2017 The Authors. Journal of Bone and Mineral Research Published by Wiley Periodicals Inc.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v33.4
    DOI: 10.1002/jbmr.3354
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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  • 10
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    GPM6B regulates osteoblast function and induction of mineralization by controlling cytoskeleton and matrix vesicle release
    Wiley ; 2011
    In:  Journal of Bone and Mineral Research Vol. 26, No. 9 ( 2011-09), p. 2045-2051
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 26, No. 9 ( 2011-09), p. 2045-2051
    Abstract: Neuronal membrane glycoprotein gene ( GPM6B ) encodes a membrane glycoprotein that belongs to the proteolipid protein family. We identified GPM6B as a gene that is strongly upregulated during osteoblast differentiation. To investigate the role of GPM6B in the process of bone formation, we silenced GPM6B expression during osteogenic differentiation of human mesenchymal stem cells (hMSCs). GPM6B silencing in hMSCs resulted in reduced alkaline phosphate (ALP) activity along with reduced mineralization of extracellular matrix (ECM). Microarray expression analysis of GPM6B ‐depleted osteogenic hMSCs revealed significant changes in genes involved in cytoskeleton organization and biogenesis. Immunocytochemistry results confirm changes in the distribution of actin filaments, as well as the shape and size of focal adhesions on GPM6B silencing. Moreover, we demonstrated that production and release of ALP‐positive matrix vesicles (MVs) were reduced. In conclusion, we identified GPM6B as a novel regulator of osteoblast function and bone formation. This finding demonstrates the significance of cytoskeleton organization for MV production and subsequent mineralization. © 2011 American Society for Bone and Mineral Research
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v26.9
    DOI: 10.1002/jbmr.435
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2011
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