ArticlePloS one2012
Targeted disruption of ephrin B1 in cells of myeloid lineage increases osteoclast differentiation and bone resorption in mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Neuronal Guidance Molecules in Bone Remodeling and Orthodontic Tooth Movement.International journal of molecular sciences · 2022Review
- Eph-Ephrin Signaling Mediates Cross-Talk Within the Bone Microenvironment.Frontiers in cell and developmental biology · 2021Review
- The EphA4 Signaling is Anti-catabolic in Synoviocytes but Pro-anabolic in Articular Chondrocytes.Calcified tissue international · 2020Article
- Novel Role for Claudin-11 in the Regulation of Osteoblasts via Modulation of ADAM10-Mediated Notch Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Skeletal effects of nongenomic thyroid hormone receptor beta signaling.The Journal of endocrinology · 2019Article
- Changes in ephrin gene expression during bone healing identify a restricted repertoire of ephrins mediating fracture repair.Histochemistry and cell biology · 2019Article
- Vitamin C effects on 5-hydroxymethylcytosine and gene expression in osteoblasts and chondrocytes: Potential involvement of PHD2.PloS one · 2019Article
- A novel miR17/protein tyrosine phosphatase-oc/EphA4 regulatory axis of osteoclast activity.Archives of biochemistry and biophysics · 2018Review
- Role of IGF1 and EFN-EPH signaling in skeletal metabolism.Journal of molecular endocrinology · 2018Review
- Ephrin ligands and Eph receptors contribution to hematopoiesis.Cellular and molecular life sciences : CMLS · 2017Review
- IGF-1 Mediates EphrinB1 Activation in Regulating Tertiary Dentin Formation.Journal of dental research · 2017Article
- Thyroid hormone acting via TRβ induces expression of browning genes in mouse bone marrow adipose tissue.Endocrine · 2017Article
- Conditional Deletion of the Phd2 Gene in Articular Chondrocytes Accelerates Differentiation and Reduces Articular Cartilage Thickness.Scientific reports · 2017Article
- Prolyl Hydroxylase Domain-Containing Protein 2 (Phd2) Regulates Chondrocyte Differentiation and Secondary Ossification in Mice.Scientific reports · 2016Article
- Identification of biallelic LRRK1 mutations in osteosclerotic metaphyseal dysplasia and evidence for locus heterogeneity.Journal of medical genetics · 2016Article
- Bidirectional ephrin signaling in bone.Osteoporosis and sarcopenia · 2016Review
- Mechanisms of ephrin-Eph signalling in development, physiology and disease.Nature reviews. Molecular cell biology · 2016Review
- Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice.International journal of molecular medicine · 2016Article
- Conditional Deletion of Prolyl Hydroxylase Domain-Containing Protein 2 (Phd2) Gene Reveals Its Essential Role in Chondrocyte Function and Endochondral Bone Formation.Endocrinology · 2016Article
- Early molecular responses of bone to estrogen deficiency induced by ovariectomy in rats.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Disruption of ephrin B1 in collagen I producing cells in mice results in severe skull defects and reduced bone formation. Because ephrin B1 is also expressed during osteoclast differentiation and because little is known on the role of ephrin B1 reverse signaling in bone resorption, we examined the bone phenotypes in ephrin B1 conditional knockout mice, and studied the function of ephrin B1 reverse signaling on osteoclast differentiation and resorptive activity. Targeted deletion of ephrin B1 gene in myeloid lineage cells resulted in reduced trabecular bone volume, trabecular number and trabecular thickness caused by increased TRAP positive osteoclasts and bone resorption. Histomorphometric analyses found bone formation parameters were not changed in ephrin B1 knockout mice. Treatment of wild-type precursors with clustered soluble EphB2-Fc inhibited RANKL induced formation of multinucleated osteoclasts, and bone resorption pits. The same treatment of ephrin B1 deficient precursors had little effect on osteoclast differentiation and pit formation. Similarly, activation of ephrin B1 reverse signaling by EphB2-Fc treatment led to inhibition of TRAP, cathepsin K and NFATc1 mRNA expression in osteoclasts derived from wild-type mice but not conditional knockout mice. Immunoprecipitation with NHERF1 antibody revealed ephrin B1 interacted with NHERF1 in differentiated osteoclasts. Treatment of osteoclasts with exogenous EphB2-Fc resulted in reduced phosphorylation of ezrin/radixin/moesin. We conclude that myeloid lineage produced ephrin B1 is a negative regulator of bone resorption in vivo, and that activation of ephrin B1 reverse signaling inhibits osteoclast differentiation in vitro in part via a mechanism that involves inhibition of NFATc1 expression and modulation of phosphorylation status of ezrin/radixin/moesin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.