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Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism
Open accessAbstract
The osteocyte, a terminally differentiated cell comprising 90%-95% of all bone cells, may have multiple functions, including acting as a mechanosensor in bone (re)modeling. Dentin matrix protein 1 (encoded by DMP1) is highly expressed in osteocytes and, when deleted in mice, results in a hypomineralized bone phenotype. We investigated the potential for this gene not only to direct skeletal mineralization but also to regulate phosphate (P(i)) homeostasis. Both Dmp1-null mice and individuals with a newly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting associated with elevated fibroblast growth factor 23 (FGF23) levels and normocalciuria. Mutational analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affecting the DMP1 start codon, and a second family carried a 7-bp deletion disrupting the highly conserved DMP1 C terminus. Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization. Our findings suggest a bone-renal axis that is central to guiding proper mineral metabolism.
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“Impaired DMP1 function is associated with a hypomineralized bone phenotype, which can result in rickets or osteomalacia 40,41 .”
From Sex-specific gene expression signatures of calcific aortic valve stenosis in a large collection of human tissues (2026) · cites this paper as [41]
In the citing paper
“Mutations in genes that have highly enriched expression in osteocytes cause rare bone and mineral disorders.”
From Osteocyte transcriptome mapping identifies a molecular landscape controlling skeletal homeostasis and susceptibility to skeletal disease (2021) · cites this paper as [20]
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Cites
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“The loss of DMP1 function in humans and mice results in autosomal recessive hypophosphatemic rickets/osteomalacia (ARHR), characterized by defects in odontoblast and osteoblast differentiation, matrix mineralization and hypophosphatemia resulting from elevated levels of circulating fibroblast growth factor 23 (FGF23),…”
BackgroundSelf-citationThe Specific Role of FAM20C in Dentinogenesis
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BackgroundEvocalcet Rescues Secondary Hyperparathyroidism-driven Cortical Porosity in CKD Male Rats
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BackgroundAdvances in the research on myokine-driven regulation of bone metabolism
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BackgroundNon-Classical Effects of FGF23: Molecular and Clinical Features
Martínez-Heredia, L., Moreno, J. M. C., García-Fontana, B., & Muñoz‐Torres, M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094875 · Cited by 37
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“ARHR1 (OMIM #241520) is caused by mutations in Dentin Matrix Protein 1, DMP1 (Feng et al., 2006) whereas ARHR2 is caused by mutations in ectonucleotide phyrophospatase/phosphodiesterase 1, ENPP1 (Lorenz-Depiereux et al., 2010).”
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“Similarly, dmp-1 knockout mice developed hypophosphatemia because of increased bioactivities of FGF23.”
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“These include inactivating mutations in phosphate regulating endopeptidase homolog, X-Linked (PHEX), dentin matrix protein 1 (DMP1), ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) and family with sequence similarity 20, member c (FAM20C) [33].”
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“These observations suggest that Dmp1 has both a systemic- (regulation of FGF23) and a local-function (regulation of osteocyte perilacunar mineralization).”
BackgroundInfluentialSelf-citationKao, R. S., Abbott, M. J., Louie, A., O’Carroll, D., Lu, W.-D., & Nissenson, R. A. (2013) · Bone · doi:10.1016/j.bone.2013.04.001 · Cited by 29
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BackgroundThe role of cells and signal pathways in subchondral bone in osteoarthritis
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3D Printing Hierarchical Porous Nanofibrous Scaffold for Bone Regeneration
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Extracellular Phosphate, Inflammation and Cytotoxicity
Michigami, T., Yamazaki, M., & Razzaque, M. S. (2022) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-91623-7_3 · Cited by 27
Targeting osteocytes vs osteoblasts
Kitase, Y., & Prideaux, M. (2023) · Bone · doi:10.1016/j.bone.2023.116724 · Cited by 30
The changing face of hypophosphatemic disorders in the FGF-23 era.
Lee, J. Y., & Imel, E. A. (2013) · PubMed · Cited by 26
Steroid-Associated Hip Joint Collapse in Bipedal Emus
Zheng, L.-Z., Liu, Z., Lei, M., Peng, J., He, Y.-X., Xie, X.-H., Man, G. C. W., Huang, L., Wang, X.-L., Fong, D. T.-P., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0076797 · Cited by 26
“The samples were then sputtercoated with gold and palladium, as described previously [40,41] and examined for bone matrix and features of osteocytes in the scanning electron microscope (SEM) (JSM-6300, JEOL, Japan).”
MethodSelf-citationPeriodontal Status of Patients With Hypophosphatemic Rickets: A Case Series
Ye, L., Liu, R., White, N., Alon, U. S., & Cobb, C. M. (2011) · Journal of Periodontology · doi:10.1902/jop.2011.100736 · Cited by 26
FGF23: a key player in mineral and bone disorder in CKD.
Komaba, H., & Fukagawa, M. (2009) · PubMed · doi:10.3265/nefrologia.2009.29.5.5400.en.full · Cited by 26
Liu, X., Li, Q., Wang, F., & Wang, Z. (2016) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2016.01.004 · Cited by 26
“hypophosphatemic rickets, and novel human disorder (Feng et al., 2006; Ye et al., 2004, 2005).”
BackgroundGlycosylation of DMP1 Is Essential for Chondrogenesis of Condylar Cartilage
Weng, Y., Liu, Y., Du, H., Li, L., Jing, B., Zhang, Q., Wang, X., Wang, Z., & Sun, Y. (2017) · Journal of Dental Research · doi:10.1177/0022034517717485 · Cited by 26
“It is well known that DMP1 plays critical roles in dentinogenesis and osteogenesis (Ye, MacDougall, et al. 2004; Feng et al. 2006).”
BackgroundKlein‐Nulend, J., & Bonewald, L. F. (2008) · Elsevier eBooks · doi:10.1016/b978-0-12-373884-4.00028-8 · Cited by 26
Self-citationPolyphosphate Nanoparticles: Balancing Energy Requirements in Tissue Regeneration Processes
Müller, W. E. G., Neufurth, M., Wang, S., Schröder, H. C., & Wang, X. (2024) · Small · doi:10.1002/smll.202309528 · Cited by 25
Mumm, S. R., Huskey, M., Cajic, A., Wollberg, V., Zhang, F., Madson, K. L., Wenkert, D., McAlister, W. H., Gottesman, G. S., & Whyte, M. P. (2014) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2307 · Cited by 25
“(23) Here, we investigated whether this 30‐UTR PHEX mutation accounts for any of our original 19 apparently sporadic XLH patients lacking mutations in the coding or splice sites of PHEX,DMP1, or FGF23, and in a further 22 “sporadic” XLH patients.”
BackgroundInfluentialFibroblast Growth Factor 23–Mediated Bone Disease
Gonciulea, A. R., & de Beur, S. M. J. (2016) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2016.09.013 · Cited by 25
Dai, G., Xiao, H., Liao, J., Zhou, N., Zhao, C., Xu, W., Xu, W., Liang, X., & Huang, W. C. (2020) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2020.4576 · Cited by 25
Graves, J. M., Vallejo, J. A., Hamill, C. S., Wang, D. D., Ahuja, R., Patel, S., Faul, C., & Wacker, M. (2021) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00798.2020 · Cited by 27
Bizzari, S., Nair, P., Deepthi, A., Hana, S., Al‐Ali, M. T., Mégarbané, A., & El‐Hayek, S. (2021) · Genes · doi:10.3390/genes12101518 · Cited by 25
Increased trabecular bone formation in mice lacking the growth factor midkine
Neunaber, C., Catalá-Lehnen, P., Beil, F. T., Marshall, R. P., Kanbach, V., Baranowsky, A., Lehmann, W., Streichert, T., Ignatius, A. A., Muramatsu, T., et al. (2010) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.75 · Cited by 25
“In fact, Dmp1 has been demonstrated to be required for both proper bone matrix mineralization and the regulation of phosphate homeostasis.((36,37)) Thus, based on our molecular analysis, we particularly analyzed the Mdk-deficient mice for respective phenotypes, but we observed neither increased osteoid volume nor hypo…”
BackgroundBone cell–matrix protein interactions
Marie, P. J. (2009) · Osteoporosis International · doi:10.1007/s00198-009-0856-7 · Cited by 25
“DMP-1 knockout results in hypomineralization due to elevated FGF-23 production and subsequent defective phosphate reabsorption by the kidney [54].”
BackgroundInduction of an osteocyte-like phenotype by fibroblast growth factor-2
Gupta, R. R., Yoo, D. J., HEBERT, C. A., Niger, C., & Stains, J. P. (2010) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2010.10.011 · Cited by 25
“Underscoring its physiologic relevance in osteocyte and skeletal biology, genetic ablation of DMP1 in mice results in osteomalacia and hypophosphatemia, as well as, defective osteocyte differentiation and a disorganized osteocyte lacuno-canalicular network [33].”
BackgroundQuarles, L. D. (2013) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2012.12.014 · Cited by 25
Self-citationSun, Y., Ma, S., Zhou, J. R., Yamoah, A. K., Feng, J. Q., Hinton, R. J., & Qin, C. (2010) · Journal of Histochemistry & Cytochemistry · doi:10.1369/jhc.2010.956771 · Cited by 25
“The importance of DMP1 for dentin and bone mineralization has been demonstrated by in vitro mineralization studies (Gericke et al. 2010), gene ablation experiments in mice (Ye et al. 2004,2005), and human genetic studies (Feng et al. 2006).”
BackgroundSelf-citationRen, Y., Han, X., Jing, Y., Yuan, B., Ke, H.-Z., Liu, M., & Feng, J. Q. (2015) · Matrix Biology · doi:10.1016/j.matbio.2015.12.009 · Cited by 25
“Twenty-μm sections were cut and stained for Masson Goldner trichrome staining as previously described[6]; bioquant (Nashville, TN) was used to quantify the osteoid/mineralized bone areas and ratios.”
BackgroundMethodInfluentialSelf-citationNoncollagenous Bone Matrix Proteins
Robey, P. G. (2008) · Elsevier eBooks · doi:10.1016/b978-0-12-373884-4.00036-7 · Cited by 25
Mineralization processes in hard tissue
An, J., Leeuwenburgh, S. C. G., Wolke, J. G. C., & Jansen, J. A. (2016) · Elsevier eBooks · doi:10.1016/b978-1-78242-338-6.00005-3 · Cited by 29
Jing, Y., Wang, Z., Li, H., Ma, C., & Feng, J. Q. (2020) · Current Osteoporosis Reports · doi:10.1007/s11914-020-00586-3 · Cited by 25
Self-citationChen, S., Xie, W., Liu, Z., Shan, H., Chen, M., Song, Y., Yu, H., Lai, L., & Li, Z. (2020) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2020.07.037 · Cited by 26
Role of Cell Death in Cellular Processes During Odontogenesis
Abramyan, J., Geetha‐Loganathan, P., Šulcová, M., & Buchtová, M. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.671475 · Cited by 25
Osteocytes Enhance Osteogenesis by Autophagy-Mediated FGF23 Secretion Under Mechanical Tension
Xu, H., Xia, M., Sun, L., Wang, H., & Zhang, W. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.782736 · Cited by 26
“FGF23 is recognized as an important regulator of phosphate and calcium homeostasis and is mainly secreted by osteocytes (Feng et al., 2006; Edmonston and Wolf, 2020)Therefore, to determine if autophagy affects osteoblast function via protein secretion, we evaluated FGF23 expression in MLO-Y4 cells.”
BackgroundRegulation of bone metabolism by nuclear receptors
Imai, Y., Kondoh, S., Kouzmenko, A., & Kato, S. (2008) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2008.08.015 · Cited by 25
Osteocytes: Mechanosensors of Bone and Orchestrators of Mechanical Adaptation
Klein‐Nulend, J., & Bakker, A. D. (2007) · Clinical Reviews in Bone and Mineral Metabolism · doi:10.1007/s12018-008-9014-6 · Cited by 25
“DMP1 is specifically expressed along and in the canaliculi of osteocytes within the bone matrix [ 23 ].”
BackgroundInfluentialPhulwani, P., Bergwitz, C., Jaureguiberry, G., Rasoulpour, M., & Estrada, E. (2011) · American Journal of Medical Genetics Part A · doi:10.1002/ajmg.a.33832 · Cited by 24
“…autosomal dominant hypophosphatemic rickets [Econs et al., 1997] (ADHR, OMIM 193100, FGF23 gene mutations), autosomal recessive hypophosphatemia [Feng et al., 2006; Lorenz-Depiereux et al., 2006a] (ARHP, OMIM 241520, DMP1 gene mutations), and autosomal recessive hypophosphatemic rickets with…”
BackgroundBertrand, S., Fuentealba, J. R., Aze, A., Hudson, C., Yasuo, H., Torrejón, M., Escrivá, H., & Marcellini, S. (2013) · Proceedings of the Royal Society B Biological Sciences · doi:10.1098/rspb.2012.2963 · Cited by 26
Bone Development and Remodeling
Maes, C., & Kronenberg, H. M. (2015) · Elsevier eBooks · doi:10.1016/b978-0-323-18907-1.00060-3 · Cited by 26
Fricain, J., Aid, R., Lanouar, S., Maurel, D. B., Nihouannen, D. L., Delmond, S., Letourneur, D., Amédée, J., & Catros, S. (2018) · Dental Materials · doi:10.1016/j.dental.2018.03.021 · Cited by 24
Hasegawa, T., Amizuka, N., Yamada, T., Liu, Z., Miyamoto, Y., Yamamoto, T., Sasaki, M., Hongo, H., Suzuki, R., de Freitas, P. H. L., et al. (2013) · Biomedical Research · doi:10.2220/biomedres.34.153 · Cited by 24
Bone anatomy, physiology and adaptation to mechanical loading
Fuchs, R. K., Warden, S. J., & Turner, C. H. (2009) · Elsevier eBooks · doi:10.1533/9781845696610.1.25 · Cited by 32
Metadata
- Authors
- Feng, J. Q., Ward, L. M., Liu, S., Lu, Y., Xie, Y., Yuan, B., Yu, X., Rauch, F., Davis, S. I., Zhang, S., Rios, H., Drezner, M. K., Quarles, L. D., Bonewald, L. F., & White, K. E.
- Affiliations
- University of Missouri–Kansas City (US)
- University of Ottawa (CA)
- University of Kansas (US)
- University of Wisconsin–Madison (US)
- Indiana University Indianapolis (US)
- McGill University (CA)
- Corresponding author
- Ward, Leanne M
- Quarles, L Darryl
- ORCID
- Venue
- Nature Genetics
- Published
- 2006-10-08
- Volume
- 38
- Issue
- 11
- Pages
- 1310-1315
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC1839871
- OpenAlex
- W2051959338
- Cited by
- 1,199
- References
- 25
- Citations by year
- 2026: 29 · 2025: 19 · 2024: 31 · 2023: 47 · 2022: 60 · 2021: 59 · 2020: 61 · 2019: 63 · 2018: 62 · 2017: 57 · 2016: 52 · 2015: 64 · 2014: 58 · 2013: 81 · 2012: 93
- FWCI
- 46.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK063934, R01DK063934)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR045955, R01AR051587, AR 046798, R01AR027032, AR027032, R56AR045955, R56AR027032, P01AR046798, AR051587, AR-45955)
- National Institute of Dental and Craniofacial Research (DE 13480, R29DE013480)
- Topics
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Alkaline Phosphatase Research Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- DMP1, osteocytes, rickets, osteomalacia, phosphate homeostasis, fibroblast growth factor 23, bone mineralization, renal phosphate wasting, start codon mutation, C-terminal deletion
- MeSH terms
- Fibroblast Growth Factor-23, Adult, Animals, Bone and Bones, Calcification, Physiologic, Cells, Cultured, DNA Mutational Analysis, Female, Fibroblast Growth Factors, Humans, Kidney, Male, Mice, Inbred C57BL, Minerals, Osteocytes, Osteomalacia, Phosphates, Phosphoproteins, Rickets, Extracellular Matrix Proteins, Mice, Knockout, Mice
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