Journal of Bone and Mineral Research

Cover image for Vol. 32 Issue 10

Edited By: Juliet E Compston

Impact Factor: 6.284

ISI Journal Citation Reports © Ranking: 2016: 14/138 (Endocrinology & Metabolism); 15/138 (ENDOCRINOLOGY & METABOLISM)

Online ISSN: 1523-4681

Associated Title(s): JBMR Plus

Featured

  • Cartilage-Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK-ATF4-CHOP–Dependent Manner

    Cartilage‐Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK‐ATF4‐CHOP–Dependent Manner

    Effects of Atg7 ablation on body growth, long-bone growth, and tibial growth plate histology. The Atg7 gene was ablated from chondrocytes by using a tamoxifen-inducible Cre-loxP system under the control of type II collagen promoter (Col2a-CreERTM) in a chondrocyte-specific and temporally-controlled manner. (A–C) Whole-body length (from nose to anus), femur length, and tibia length were measured at 1, 2, 4, and 8 weeks of age (n = 6/group). (D) Representative images of femur and tibia at 4 and 8 weeks of age from control and Atg7cKO mice. H&E staining of tibia growth plate of control and Atg7cKO mice at 4 weeks (F) and 8 weeks (H) of age and the growth plate zone heights were quantitatively analyzed, respectively (E, G) (n = 6/group). Scale bars = 100 µm. Data are expressed as means ± SE in each bar graph. *p < 0.05, **p < 0.01. P zone = proliferative zone; H zone = hypertrophic zone.

  • Bone Mass Is Compromised by the Chemotherapeutic Trabectedin in Association With Effects on Osteoblasts and Macrophage Efferocytosis

    Bone Mass Is Compromised by the Chemotherapeutic Trabectedin in Association With Effects on Osteoblasts and Macrophage Efferocytosis

    Reduced macrophage efferocytosis with trabectedin in vitro. (A) Marrow was extracted from 4-week-old to 8-week-old C57BL/6J mice, and macrophages expanded with M-CSF for 1 week. MC4 cells were stained red via DeepRedCell tracker dye, induced to apoptosis by UV light, and subsequently added to macrophages that were treated with trabectedin or vehicle. Macrophages were subsequently stained for F4/80 with an FITC fluorophore. (B) Efferocytosis was assessed by double-positive F4/80 and apoptotic MC4 cells, and efferocytosis was reduced by trabectedin pretreatment at a dose (2.5nM, 12 hours) that did not affect (C) macrophage viability (n = 6 to 9/group). (D) Macrophages secreted significantly more osteoinductive TGF-β with efferocytosis, and this increase was inhibited by trabectedin (10nM, 24 hours) in vitro as assessed by ELISA (n = 3/group). Data are mean ± SD. *p < 0.05 versus Veh. Veh = vehicle.

  • Integrin-Linked Kinase Regulates Bone Formation by Controlling Cytoskeletal Organization and Modulating BMP and Wnt Signaling in Osteoprogenitors

    Integrin‐Linked Kinase Regulates Bone Formation by Controlling Cytoskeletal Organization and Modulating BMP and Wnt Signaling in Osteoprogenitors

    ILK expression and inactivation in Osx+ osteoprogenitors. (A) Relative mRNA expression levels as determined by qRT-PCR of the osteoblast marker genes Osx, Opn, and Ocn (left graph), and of the integrin signaling components Itgβ1, FAK, and ILK (right graph), in FACS-sorted cell populations derived from long bones of newborn mice. Osx-Cre:GFP– and Osx-Cre:GFP+ cell fractions were collected from Osx-Cre:GFP-expressing pups (n = 5), and a parallel “full digest” control sample was harvested from Osx-Cre:GFP-negative littermates (n = 3). Bars represent the mean ± SE. Significant differences are indicated as *p < 0.05 and **p < 0.01, by one-way ANOVA followed by Tukey multiple comparison test (Itgβ1 and FAK), or Kruskal-Wallis test (Osx, Opn, Ocn, ILK). (B) Relative ILK mRNA expression level in Osx-Cre:GFP+ cells isolated by FACS from long bones of newborn control and ILK cKO pups (including per genotype n = 3 independent cell pools isolated from 4 to 6 pups each). Bars represent the mean ± SE. **p < 0.01, Student's t test. (C, D) Immunofluorescent staining for ILK (red detection) and GFP (green) in tibias of (C) embryonic (E16.5) and (D) adult (12-week-old) control and ILK cKO mice. Nuclei are stained by Hoechst (blue). Yellow arrowheads point at Osx-Cre:GFP+ cells, which are mostly GFP+/ILK+ double positive cells in control sections but lack the ILK signal in ILK cKO mice; white arrowheads indicate Osx-Cre:GFP-negative cells expressing ILK in both genotypes. POC = primary ossification center; tb = trabecular bone; GP = growth plate. Scale bars = 50 μm.

  • Therapeutic Effects of FGF23 c-tail Fc in a Murine Preclinical Model of X-Linked Hypophosphatemia Via the Selective Modulation of Phosphate Reabsorption

    Therapeutic Effects of FGF23 c‐tail Fc in a Murine Preclinical Model of X‐Linked Hypophosphatemia Via the Selective Modulation of Phosphate Reabsorption

    Dose-responsive improvement in bone architecture is evident upon treatment with FGF23 c-tail Fc hematoxylin and eosin staining of tibial physes depicts bone architecture. Images are representative of microscopic findings in the following groups: C57BL/6 control (n = 10 mice); C57BL/6J-PhexHyp/J control (n = 10 mice); C57BL/6J-PhexHyp/J 3 mg/kg/dose (n = 10 mice); C57BL/6J-PhexHyp/J 10 mg/kg/dose (n = 10 mice). Scale bars = 400 μm within each image.

  • Klotho Lacks an FGF23-Independent Role in Mineral Homeostasis

    Klotho Lacks an FGF23‐Independent Role in Mineral Homeostasis

    Simultaneous loss of Klotho and Fgf23 in 4-week-old Fgf23/Klotho/VDR mice recapitulates the phenotype of Fgf23/VDR and Klotho/VDR compound mutant mice. (A) Representative images, body weight, heart-to-body weight ratio, serum calcium (Ca), serum phosphate (Pi), serum sodium (Na), serum PTH, and serum 1,25(OH)2D levels; (B) von Kossa-stained paraffin sections of thoracic aorta and kidney, and hematoxylin and eosin–stained paraffin sections of lung in 4-week-old WT, VDRΔ/Δ (VDR), Fgf23–/– (Fgf23), Klotho–/– (KL), Fgf23–/–/Klotho–/–, Fgf23–/–/VDRΔ/Δ, Klotho–/–/VDRΔ/Δ, and Fgf23–/–/Klotho–/–/VDRΔ/Δ compound mutant mice. Scale bar = 100 μm. Each data point in A represents the mean ± SE of six to nine mice each. *p < 0.05 versus WT, #p < 0.05 versus VDRΔ/Δ mice, †p < 0.05 versus Fgf23–/–, Klotho–/–, and Fgf23–/–/Klotho–/– mice, ║p < 0.05 versus Fgf23–/– and Fgf23–/–/Klotho–/– mice, one-way ANOVA followed by Student-Newman-Keuls test. BW = body weight.

  • Cartilage‐Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK‐ATF4‐CHOP–Dependent Manner
  • Bone Mass Is Compromised by the Chemotherapeutic Trabectedin in Association With Effects on Osteoblasts and Macrophage Efferocytosis
  • Integrin‐Linked Kinase Regulates Bone Formation by Controlling Cytoskeletal Organization and Modulating BMP and Wnt Signaling in Osteoprogenitors
  • Therapeutic Effects of FGF23 c‐tail Fc in a Murine Preclinical Model of X‐Linked Hypophosphatemia Via the Selective Modulation of Phosphate Reabsorption
  • Klotho Lacks an FGF23‐Independent Role in Mineral Homeostasis

Just Published Articles

  1. Impaired Phosphate Tolerance Revealed With an Acute Oral Challenge

    Mandy E Turner, Christine A White, Wilma M Hopman, Emilie C Ward, Paul S Jeronimo, Michael A Adams and Rachel M Holden

    Version of Record online: 19 OCT 2017 | DOI: 10.1002/jbmr.3294

  2. Tracking the progression of osteolytic and osteosclerotic lesions in mice using serial in vivo micro-CT: Applications to the assessment of bisphosphonate treatment efficacy

    G.M. Campbell, R.J. Tower, T. Damm, P. Kneissl, A. Rambow, C. Schem, S. Tiwari and C.C. Glüer

    Accepted manuscript online: 18 OCT 2017 06:55AM EST | DOI: 10.1002/jbmr.3317

  3. Subchondral Trabecular Rod Loss and Plate Thickening in the Development of Osteoarthritis

    Yan Chen, Yizhong Hu, Y. Eric Yu, Xingjian Zhang, Tezita Watts, Bin Zhou, Ji Wang, Ting Wang, Weiwei Zhao, Kwong Yuen Chiu, Frankie K. L. Leung, Xu Cao, William W. Lu, William Macaulay, Kyle K. Nishiyama, Elizabeth Shane and X. Edward Guo

    Accepted manuscript online: 17 OCT 2017 07:37AM EST | DOI: 10.1002/jbmr.3313

  4. Prevalence of osteoporosis and low bone mass among Puerto Rican older adults

    Sabrina E. Noel, Kelsey M. Mangano, John L. Griffith, Nicole C. Wright, Bess Dawson-Hughes and Katherine L. Tucker

    Accepted manuscript online: 17 OCT 2017 06:00AM EST | DOI: 10.1002/jbmr.3315

  5. The Effect of Vitamin D Supplementation on Bone Metabolic Markers in Chronic Kidney Disease

    Ashok Kumar Yadav, Vivek Kumar, Vinod Kumar, Debasish Banerjee, Krishan Lal Gupta and Vivekanand Jha

    Accepted manuscript online: 17 OCT 2017 06:00AM EST | DOI: 10.1002/jbmr.3314

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Design Enhancements for JBMR Online

Design Enhancements for JBMR online

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JBMR® Announces Workflow Changes and Author Guidelines Updates

In response to rising concerns over the reproducibility of biomedical research, the author guidelines and submission procedures for the Journal of Bone and Mineral Research’s (JBMR®) have recently been updated. These updates affect the submission workflow of author forms required for peer review and publication, as detailed below:


ARRIVE: Authors submitting research on animal studies are now required to complete an adapted ARRIVE (Animals in Research: Reporting In Vivo Experiments) checklist at submission.


CONSORT: Authors of manuscripts reporting results of clinical trials are now required to upload the CONSORT checklist at submission.


STROBE: Authors of manuscripts reporting results of human observational case-control, cohort, or cross-sectional studies are now required to upload the STROBE checklist at submission.


Author Agreement: The conflict of interest (COI) and copyright transfer (CTA) portions of the current Author Agreement can now be completed electronically as a web form, eliminating the need for authors to print, scan and upload a PDF form upon submission.


• COI information will be collected during submission via an online questionnaire on ScholarOne.


• The CTA will be completed at manuscript acceptance: If a manuscript is accepted for publication, the corresponding author will receive an e-mail prompt to log in to Author Services. Author Services is a Wiley web application that provides production tracking, as well as other resources for authors. From this site, corresponding authors can complete the CTA on behalf of all authors on the paper.

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