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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
Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23
White, K., Evans, W. E., O'Riordan, J., Speer, M., Econs, M., Lorenz-Depiereux, B., Grabowski, M., Meitinger, T., & Strom, T. (2000) · Nature Genetics · doi:10.1038/81664 · Cited by 1,467
Self-citationFrancis, F., Hennig, S., Korn, B., Reinhardt, R., de Jong, P., Poustka, A. J., Lehrach, H. R., Rowe, P. S., Goulding, J. N., Summerfield, T. C., et al. (1995) · Nature Genetics · doi:10.1038/ng1095-130 · Cited by 1,095
Self-citationPathogenic role of Fgf23 in Hyp mice
Liu, S., Zhou, J., Tang, W., Jiang, X., Rowe, D. W., & Quarles, L. D. (2006) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00008.2006 · Cited by 494
Self-citationSix Genes Expressed in Bones and Teeth Encode the Current Members of the SIBLING Family of Proteins
Fisher, L. W., & Fedarko, N. S. (2003) · Connective Tissue Research · doi:10.1080/03008200390152061 · Cited by 467
Hypophosphatemia: mouse model for human familial hypophosphatemic (vitamin D-resistant) rickets.
Eicher, E. M., Southard, J. L., Scriver, C. R., & Glorieux, F. H. (1976) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.73.12.4667 · Cited by 405
MEPE, a New Gene Expressed in Bone Marrow and Tumors Causing Osteomalacia
Rowe, P. S., de Zoysa, P. A., Dong, R., Wang, H. R., White, K. E., Econs, M. J., & Oudet, C. L. (2000) · Genomics · doi:10.1006/geno.2000.6235 · Cited by 360
Self-citationD’Souza, R. N., Cavender, A. C., Sunavala, G., Alvarez, J., Ohshima, T., Kulkarni, A. B., & MacDougall, M. J. (1997) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.1997.12.12.2040 · Cited by 348
Normative data for iliac bone histomorphometry in growing children
Glorieux, F. H., Travers, R., Taylor, A., Bowen, J. R., Rauch, F., Norman, M., & PARFITT, A. M. (2000) · Bone · doi:10.1016/s8756-3282(99)00257-4 · Cited by 337
Self-citationZhang, K., Barragan‐Adjemian, C., Ye, L., Kotha, S. P., Dallas, M., Lu, Y., Zhao, S., Harris, M. A., Harris, S. E., Feng, J. Q., et al. (2006) · Molecular and Cellular Biology · doi:10.1128/mcb.02120-05 · Cited by 299
Self-citationYe, L., MacDougall, M. J., Zhang, S., Xie, Y., Zhang, J., Li, Z., Lu, Y., Mishina, Y. M., & Feng, J. Q. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m400490200 · Cited by 292
Self-citation
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- Feng, J.Q. et al. The Dentin matrix protein 1 (Dmp1) is specifically expressed in mineralized, but not soft tissues during development. J. Dent. Res. 82, 776–780 (2003). · DOI
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Sorted by citations
Items 601–700 of 1,001
Schiavi, S. C. (2006) · Nature Genetics · doi:10.1038/ng1106-1230 · Cited by 24
Overexpression of Dmp1 fails to rescue the bone and dentin defects inFam20Cknockout mice
Wang, X., Wang, J., Yuan, B., Lu, Y., Feng, J. Q., & Qin, C. (2014) · Connective Tissue Research · doi:10.3109/03008207.2014.923414 · Cited by 23
“These defects are very similar to those in mice with inactivated Dmp1 (4), a”
BackgroundSelf-citationThe Emerging Role of Cell Transdifferentiation in Skeletal Development and Diseases
Wang, K., Ma, C., Feng, J. Q., & Jing, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23115974 · Cited by 23
“Mutation of DMP1 in human [80,81] and deletion of DMP1 in mice [79,80] and rabbits [82] lead to defects in”
BackgroundSelf-citationUltrashort peptides induce biomineralization
Ding, Y., Cai, M., Niu, P., Zhang, H., Zhang, S., & Sun, Y. (2022) · Composites Part B Engineering · doi:10.1016/j.compositesb.2022.110196 · Cited by 23
Self-citationPTH and Vitamin D Repress DMP1 in Cementoblasts
Wang, L., Tran, A. B., Nociti, F. H., Thumbigere‐Math, V., Foster, B. L., Krieger, C. C., Kantovitz, K. R., Novince, C. M., Koh, A. J., McCauley, L. K., et al. (2015) · Journal of Dental Research · doi:10.1177/0022034515599726 · Cited by 23
Cai, J., Shao, X., Yan, Z., Liu, X., Yang, Y., Luo, E., & Jing, D. (2019) · The FASEB Journal · doi:10.1096/fj.201902779r · Cited by 22
Pazzaglia, U. E., & Congiu, T. (2012) · Journal of Anatomy · doi:10.1111/joa.12004 · Cited by 23
“…of bone with methyl-methacrylate and etching of the mineralized bone matrix have been used to obtain a visualization of the osteocyte lacunae and the system of canalicula (Marotti et al., 1985; Okada et al., 2002; Feng et al., 2006; Lu et al., 2007; Gorustovich, 2010; Kubek et al., 2010).”
MethodLu, X., Rios, H. F., Jiang, B., Xing, L., Kadlcek, R. M., Greenfield, E. M., Luo, G., & Feng, J. Q. (2009) · European Journal Of Oral Sciences · doi:10.1111/j.1600-0722.2009.00690.x · Cited by 23
“The surface of the MMA-embedded bone was polished, coated with gold and palladium, and examined using an FEI/Philips XL30 Field emission environmental scanning electron microscope (FEI/Philips, Hillsboro, OR, USA), as previously described (26).”
MethodSelf-citationInherited disorders of calcium homeostasis
Ramasamy, I. (2008) · Clinica Chimica Acta · doi:10.1016/j.cca.2008.04.011 · Cited by 23
“[240] confirmed biallelic mutations in DMP1 in ARHR individuals from two families.”
BackgroundHollberg, K., Marsell, R., Norgård, M., Larsson, T. E., Jonsson, K. B., & Andersson, G. N. (2008) · Bone · doi:10.1016/j.bone.2008.01.019 · Cited by 23
“The lack of regulation of DMP1 is particularly interesting, since DMP1 knockout mice are rachitic in conjunction with elevated levels of FGF23 [31].”
BackgroundFGF23 and Bone and Mineral Metabolism
Fukumoto, S. (2019) · Handbook of experimental pharmacology · doi:10.1007/164_2019_330 · Cited by 22
FAM20C Functions Intracellularly Within Both Ameloblasts and Odontoblasts In Vivo
Wang, S., Samann, A. C., Hu, J. C. ‐., & Simmer, J. P. (2013) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.1990 · Cited by 22
“The SCPP protein DMP1, for instance, functions in phosphate homeostasis((5)) and Fam20c null mice have hypophosphatemic rickets.”
BackgroundChi, Y., Zhao, Z., He, X., Sun, Y., Jiang, Y., Li, M., Wang, O., Xing, X., Sun, A. Y., Zhou, X., et al. (2013) · Bone · doi:10.1016/j.bone.2013.11.008 · Cited by 22
“23 (FGF23) is not elevated in HHRH, which further helps differentiate it from the FGF23-dependent hypophosphatemic disorders such as autosomal dominant hypophosphatemic rickets (ADHR; FGF23 mutation) [2], autosomal recessive hypophosphatemic rickets (ARHR; DMP1, ENPP1 mutation) [3,4], and X-linked hypophosphatemia (XL…”
BackgroundAnti-fibroblast growth factor 23 antibody therapy
Fukumoto, S. (2014) · Current Opinion in Nephrology & Hypertension · doi:10.1097/01.mnh.0000447012.98357.da · Cited by 22
“Because mutations in DMP1 were shown to be responsible for autosomal recessive hypophosphatemic rickets 1 (ARHR1) [19,20], another FGF23-related hypophosphatemic rickets, it is possible that mutant FAM20C proteins induced FGF23 overexpression by modulating functions of DMP1. thorized reproduction of this article is pr…”
BackgroundRegulation of Hormone-Sensitive Renal Phosphate Transport
Gattineni, J., & Friedman, P. A. (2015) · Vitamins and hormones · doi:10.1016/bs.vh.2015.01.002 · Cited by 23
Merkel, A. C., Chen, Y., & George, A. (2019) · Frontiers in Physiology · doi:10.3389/fphys.2019.01175 · Cited by 22
“We and others have demonstrated the role of DMP1 in the formation of mineralized tissues (Feng et al., 2006; George et al., 2018).”
BackgroundKatô, H., Hidaka, N., Koga, M., Ogawa, N., Takahashi, S., Miyazaki, H., Nangaku, M., Makita, N., & Ito, N. (2021) · Journal of Bone and Mineral Metabolism · doi:10.1007/s00774-021-01258-7 · Cited by 22
Raina, R. (2012) · Journal of Nephrology & Therapeutics · doi:10.4172/2161-0959.s3-008 · Cited by 22
Porcine dentin sialoprotein glycosylation and glycosaminoglycan attachments
Yamakoshi, Y., Nagano, T., Hu, J. C. ‐., Yamakoshi, F., & Simmer, J. P. (2011) · BMC Biochemistry · doi:10.1186/1471-2091-12-6 · Cited by 22
“Dentin matrix protein 1 (Dmp1) is a bone and dentin proteoglycan that plays a role in phosphate homeostasis [52].”
BackgroundLiu, G., Wei, J., Xiao, W., Xie, W., Ru, Q., Chen, L., Wu, Y., Mobasheri, A., & Li, Y. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115884 · Cited by 23
Dey, P. (2020) · IntechOpen eBooks · doi:10.5772/intechopen.92065 · Cited by 21
Roles of osteocytes in phosphate metabolism
Michigami, T. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.967774 · Cited by 22
“Frontiers in Endocrinology 03 Studies using Phex-deficient hypophosphatemic Hyp mice and Dmp1-null mice have suggested that enhanced FGFR signaling in osteocytes contributes to the increased production of FGF23 in XLH and ARHR1 (8, 28, 29).”
BackgroundCCL7 Is a Protective Factor Secreted by Mechanically Loaded Osteocytes
Kitase, Y., Lee, S., Gluhak‐Heinrich, J., Johnson, M. L., Harris, S. E., & Bonewald, L. F. (2014) · Journal of Dental Research · doi:10.1177/0022034514553008 · Cited by 20
“Osteocytes regulate mineral homeostasis both locally and systematically (Feng et al., 2006; Liu et al., 2006) and orchestrate osteoblast and osteoclast activity in response to mechanical stimuli to regulate bone formation and resorption (Li et al., 2008; Nakashima et al., 2011).”
BackgroundSelf-citationTranscriptional regulation of dentin matrix protein 1 (DMP1) in odontoblasts and osteoblasts
Jacob, A., Zhang, Y., & George, A. (2014) · Connective Tissue Research · doi:10.3109/03008207.2014.923850 · Cited by 21
“DMP1 knockout mice display predominant skeletal defects, implying a regulatory role in osteoblast differentiation and matrix mineralization (4).”
BackgroundHypophosphatemic Rickets: Unraveling the Role of FGF23
Pettifor, J. M., & Thandrayen, K. (2012) · Calcified Tissue International · doi:10.1007/s00223-012-9651-0 · Cited by 21
“Autosomal recessive hypophosphatemic rickets 241520 [23] DMP1 Inactivating mutation in DMP1 (involved in mineralization) Increased Within normal range”
BackgroundHolecki, M. T., Chudek, J. T., Więcek, A., Titz-Bober, M., & Duława, J. (2011) · International Journal of Endocrinology · doi:10.1155/2011/707126 · Cited by 21
“Hindawi Publishing Corporation International Journal of Endocrinology Volume 2011, Article ID 707126, 5 pages doi:10.1155/2011/707126”
BackgroundInfluentialWhyte, M. P., Amalnath, S. D., McAlister, W. H., McKee, M. D., Novack, D. V., Huskey, M., Duan, S., Bijanki, V. N., Alur, S., & Mumm, S. R. (2019) · Bone · doi:10.1016/j.bone.2019.115190 · Cited by 21
“The etiology of ARHR1 was discovered in 2006 in three families by Lorenz-Depiereux et al(4) and in two families by Feng et al.(5) Turan et al(8) in 2010 detailed the findings of three affected children.”
BackgroundThe role of fibroblast growth factor 23 in chronic kidney disease-mineral and bone disorder.
Diniz, H., & Frazão, J. M. (2013) · PubMed · doi:10.3265/nefrologia.pre2013.jul.12091 · Cited by 21
Stress Chaperone GRP-78 Functions in Mineralized Matrix Formation
Ravindran, S., Gao, Q., Ramachandran, A., Blond, S. Y., Predescu, S. A., & George, A. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.179341 · Cited by 21
Generation of a conditional null allele for Dmp1 in mouse
Feng, J. Q., Scott, G. J., Guo, D., Jiang, B., Harris, M. A., Ward, T., Ray, M. K., Bonewald, L. F., Harris, S. E., & Mishina, Y. M. (2008) · genesis · doi:10.1002/dvg.20370 · Cited by 21
“…of DMP1 mutations in patients with autosomal recessive hypophosphatemia rickets not only shows the clinical relevance of DMP1 in human disease, but also extends the function of bone to that of an endocrine organ that regulates Pi homeostasis (Feng et al., 2006; Lorenz-Depiereux et al., 2006).”
BackgroundSelf-citationNakouzi, G. A., Kreidieh, K., & Yazbek, S. N. (2014) · Journal of Community Genetics · doi:10.1007/s12687-014-0203-3 · Cited by 21
Familial Hypophosphatemia and Related Disorders
Holm, I. A., Econs, M. J., & Carpenter, T. O. (2011) · Elsevier eBooks · doi:10.1016/b978-0-12-382040-2.10026-7 · Cited by 21
Disorders of Mineral Homeostasis in the Newborn, Infant, Child, and Adolescent
Root, A. W., & Diamond, F. (2008) · Elsevier eBooks · doi:10.1016/b978-141604090-3.50022-3 · Cited by 20
Cebeci, A. N., Zou, M., BinEssa, H. A., Alzahrani, A. S., Al‐Rijjal, R. A., Al-Enezi, A. F., Al-Mohanna, F. A., Cavalier, E., Meyer, B. F., & Shi, Y. (2019) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgz260 · Cited by 20
Salivary phosphate as a biomarker for human diseases
Razzaque, M. S. (2021) · FASEB BioAdvances · doi:10.1096/fba.2021-00104 · Cited by 20
Advances in understanding of phosphate homeostasis and related disorders
Michigami, T. (2022) · Endocrine Journal · doi:10.1507/endocrj.ej22-0239 · Cited by 23
“Autosomal recessive hypophosphatemic rickets type 1 (ARHR1) and type 2 (ARHR2) are caused by biallelic inactivating variants in the dentin matrix protein 1 (DMP1) and ectonucleotide pyrophosphatase/phospho‐ diesterase 1 (ENPP1) genes, respectively, and show hypophosphatemia associated with elevated levels of FGF23 [77…”
BackgroundBurosumab Treatment for Autosomal Recessive Hypophosphatemic Rickets Type 1 (ARHR1)
Bai, X., Levental, M., & Karaplis, A. C. (2022) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgac433 · Cited by 20
Hanai, A., Kawabata, A., Nakajima, K., Masuda, K., Urakawa, I., Abe, M., Yamazaki, Y., & Fukumoto, S. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1102751 · Cited by 20
“Autosomal recessive hypophosphatemic rickets 1 is caused by mutations in the DMP1 gene (Feng et al., 2006; Lorenz-Depiereux et al., 2006).”
BackgroundMasuki, H., Li, M., Hasegawa, T., Suzuki, R., Guo, Y., Liu, Z., Oda, K., Yamamoto, T., Kawanami, M., & Amizuka, N. (2010) · Biomedical Research · doi:10.2220/biomedres.31.307 · Cited by 20
“They may also regulate bone remodeling (16, 22, 27) and mineral metabolism (4, 10, 27).”
BackgroundFibroblast growth factor 23 in chronic kidney disease: New insights and clinical implications
Damasiewicz, M. J., Toussaint, N. D., & Polkinghorne, K. R. (2011) · Nephrology · doi:10.1111/j.1440-1797.2011.01443.x · Cited by 21
“The postulated phosphaturic circulating factor was subsequently identified as FGF-23 and the characteristic phenotypes in patients with conditions of FGF-23 excess or deficiency provided important early clues regarding its function.(9,10) The FGFs are a family of polypeptides that share a common region of amino acids,…”
BackgroundChan, W. C. W., Tsang, K. Y., Cheng, Y., Ng, V. C. W., Chik, H., Tan, Z., Boot-Handford, R., BOYDE, A., Cheung, K., Cheah, K. S. E., et al. (2017) · Human Molecular Genetics · doi:10.1093/hmg/ddx339 · Cited by 20
Fulzele, K. S., Dedic, C., Lai, F., Bouxsein, M., Lotinun, S., Baron, R., & Pajevic, P. D. (2018) · Bone · doi:10.1016/j.bone.2018.09.021 · Cited by 20
“Mice lacking Gsα and osteocytes are severely osteopenic We have previously generated mice lacking Gsα in osteocytes by mating Gsα(flox/flox) mice (31) with mice expressing Cre-recombinase driven by dentin matrix protein 1 (DMP1) (23, 24, 32).”
BackgroundPires, G. O., Vieira, I. O., Hernandes, F. R., Teixeira, A. L., Oliveira, I. B., Dominguez, W. V., dos Reis, L. M., Montenegro, F. L. D. M., Moysés, R. M. A., Carvalho, A. B., et al. (2019) · Bone · doi:10.1016/j.bone.2019.01.029 · Cited by 20
Fibroblast growth factor 23 and phosphate homeostasis
Balani, S. S., & Perwad, F. (2019) · Current Opinion in Nephrology & Hypertension · doi:10.1097/mnh.0000000000000526 · Cited by 20
Jähn, K., & Zimmermann, E. A. (2021) · Current Osteoporosis Reports · doi:10.1007/s11914-021-00686-8 · Cited by 18
Induction of FGF23-related hypophosphatemic osteomalacia by alcohol consumption
Hidaka, N., Katô, H., Koga, M., Katsura, M., Oyama, Y., Kinoshita, Y., Fukumoto, S., Makita, N., Nangaku, M., & Ito, N. (2021) · Bone Reports · doi:10.1016/j.bonr.2021.101144 · Cited by 20
Biological role of heparan sulfate in osteogenesis: A review
Xu, Z., Chen, S., Feng, D., Liu, Y., Wang, Q., Gao, T., Liu, Z., Zhang, Y., Chen, J., & Qiu, L. (2021) · Carbohydrate Polymers · doi:10.1016/j.carbpol.2021.118490 · Cited by 23
PHEX Mimetic (SPR4-Peptide) Corrects and Improves HYP and Wild Type Mice Energy-Metabolism
Zelenchuk, L. V., Hedge, A.-M., & Rowe, P. S. (2014) · PLoS ONE · doi:10.1371/journal.pone.0097326 · Cited by 18
“Mutations in DMP-1 are responsible for autosomal recessive hypophosphatemic rickets (ARHR-1) a disease that has an overlapping pathophysiology with HYP [68,69].”
Seitz, S. A., Barvencik, F., Gebauer, M., Albers, J., Schulze, J., Streichert, T., Amling, M., & Schinke, T. (2010) · Calcified Tissue International · doi:10.1007/s00223-010-9344-5 · Cited by 19
“This is probably best underscored by the facts that mice lacking the SIBLING protein Dmp1 (dentin matrix protein 1) display severe defects of bone matrix mineralization and that inactivating mutations of the human DMP1 gene cause autosomal dominant hypophosphatemic rickets [46, 47].”
BackgroundRegulation of bone resorption and mineral homeostasis by osteocytes
Pajevic, P. D. (2009) · IBMS BoneKEy · doi:10.1138/20090363 · Cited by 23
“Osteocytes appear to be centrally involved in phosphate homeostasis, as suggested by recent work (3;4) reporting that loss of DMP1 in humans and in mice causes rickets, osteomalacia and severe hypophosphatemia.”
BackgroundHypophosphatemic rickets due to perturbations in renal tubular function
Penido, M. G. M. G., & Alon, U. S. (2013) · Pediatric Nephrology · doi:10.1007/s00467-013-2466-z · Cited by 19
“It is caused by mutations in the gene that encodes dentin matrix acidic phosphoprotein 1 (DMP1) that by itself does not directly affect renal phosphate handling but normally suppresses FGF-23 secretion [54].”
BackgroundYang, D., Anderson, P., Wijenayaka, A. R., Barratt, K. R., Triliana, R., Stapledon, C. J. M., Zhou, H., Findlay, D. M., Morris, H. A., & Atkins, G. J. (2017) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2017.09.005 · Cited by 19
Ma, C., Jing, Y., Li, H., Wang, K., Wang, Z., Xu, C., Sun, X., Kaji, D. A., Han, X., Huang, A. H., et al. (2020) · Bone · doi:10.1016/j.bone.2020.115687 · Cited by 18
Self-citationBetween a rock and a hard place: Regulation of mineralization in the periodontium
Andras, N. L., Mohamed, F. F., Chu, E. Y., & Foster, B. L. (2022) · genesis · doi:10.1002/dvg.23474 · Cited by 18
“Vitamin D regulates Pi and Ca 2+ metabolism and is affected by the derange- ment of FGF23 signaling (as described above for XLH, ARHR1, and HFTC), therefore we include it in this section on Pi metabolism.”
BackgroundInfluentialOsteocytes and the pathogenesis of hypophosphatemic rickets
Yamazaki, M., & Michigami, T. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1005189 · Cited by 20
“Dmp1-null mice show phenotypes reproducing the clinical manifestation in ARHR1 and exhibit defective osteocyte maturation, increased FGF23 expression in osteocytes, and impaired skeletal mineralization (56).”
BackgroundIzumikawa, M., Hayashi, K., Polan, M. A. A., Tang, J., & Saito, T. (2012) · The Scientific World JOURNAL · doi:10.1100/2012/879731 · Cited by 19
“Moreover, DMP-1 is shown to be a bone matrix protein expressed in osteoblasts and osteocytes and is assumed to play a role in bone mineral homeostasis due to its high calcium ionbinding capacity [43].”
Atkins, G. J., Findlay, D. M., Anderson, P., & Morris, H. A. (2005) · Elsevier eBooks · doi:10.1016/b978-012252687-9/50044-9 · Cited by 19
Disorders of mineral homeostasis in children and adolescents
Root, A. W., & Diamond, F. (2014) · Elsevier eBooks · doi:10.1016/b978-1-4557-4858-7.00027-5 · Cited by 18
Osteocytes in the pathogenesis of osteoporosis
Ikeda, K. (2008) · Geriatrics and gerontology international/Geriatrics & gerontology international · doi:10.1111/j.1447-0594.2008.00481.x · Cited by 19
Pre-odontoblasts, Odontoblasts, or “Odontocytes”
Larmas, M. (2008) · Journal of Dental Research · doi:10.1177/154405910808700310 · Cited by 19
“Next, we examined and compared the expression pattern of E-11, a marker for newly formed osteocytes (Feng et al., 2006; Zhang et al., 2006), in both tooth and bone.”
BackgroundYashiro, M., Ohya, M., Mima, T., Nakashima, Y., Kawakami, K., Yamamoto, S., Kobayashi, S., Yano, T., Tanaka, Y., Sonou, T., et al. (2020) · Journal of Pharmaceutical and Biomedical Analysis · doi:10.1016/j.jpba.2020.113139 · Cited by 18
Pin, F., Prideaux, M., Bonewald, L. F., & Bonetto, A. (2021) · Current Osteoporosis Reports · doi:10.1007/s11914-021-00712-9 · Cited by 20
Self-citationSakamoto, E., Kitase, Y., Fitt, A. J., Zhu, Z., Awad, K. R., Brotto, M. A. P., White, K. E., Welc, S. S., Bergwitz, C., & Bonewald, L. F. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114397 · Cited by 21
Self-citationPeng, T., Huang, B., Sun, Y., Lu, Y., Bonewald, L. F., Chen, S., Butler, W. T., Feng, J. Q., D’Souza, R. N., & Qin, C. (2008) · Cells Tissues Organs · doi:10.1159/000151373 · Cited by 18
“Recent studies also demonstrated the association between mutations in the DMP1 gene and autosomal recessive hypophosphatemic rickets, a novel human disorder [Feng et al., 2006; Lorenz-Depiereux et al., 2006].”
ResultSelf-citationCircling behavior developed in Dmp1 null mice is due to bone defects in the vestibular apparatus
Lv, K., Huang, H., Lu, Y., Qin, C., Li, Z., & Feng, J. Q. (2010) · International Journal of Biological Sciences · doi:10.7150/ijbs.6.537 · Cited by 18
“Dmp1-null mice displayed a striking change in both the bone morphology and bone mineralization (16, 18, 20).”
InfluentialSelf-citationDmp1 Null Mice Develop a Unique Osteoarthritis-like Phenotype
Zhang, Q., Lin, S., Liu, Y., Yuan, B., Harris, S. E., & Feng, J. Q. (2016) · International Journal of Biological Sciences · doi:10.7150/ijbs.15833 · Cited by 18
“Our previous studies of the Dmp1 KO mice with or without Hi-P treatment mainly focused on the growth plate and long bone [13, 18].”
BackgroundMethodInfluentialSelf-citationAn improved method to assess torsional properties of rodent long bones
Nazarian, A., Entezari, V., Vartanians, V. M., Müller, R., & Snyder, B. D. (2009) · Journal of Biomechanics · doi:10.1016/j.jbiomech.2009.04.019 · Cited by 18
“…the end of the study) to induce renal osteodystrophy (Turner et al., 1996; Miller et al., 1998; Freesmeyer et al., 2001; Kazama et al., 2003; Brkovic et al., 2005; Feng et al., 2006; Jokihaara et al., 2006) (normal rodent diet contains 1.35% Ca and 1.04% P) and severe secondary hyperparathyroidism.”
BackgroundInfluentialNi, P., Clinkenbeard, E. L., Noonan, M. L., Richardville, J. M., McClintick, J. N., Hato, T., Janosevic, D., Cheng, Y., El‐Achkar, T. M., Eadon, M. T., et al. (2020) · Kidney International · doi:10.1016/j.kint.2020.10.024 · Cited by 17
Self-citationHereditary dentin defects with systemic diseases
Su, T., Zhu, Y., Wang, X., Zhu, Q., & Duan, X. (2023) · Oral Diseases · doi:10.1111/odi.14589 · Cited by 17
Dentine matrix protein 1 (DMP-1) is a marker of bone-forming tumours
Kashima, T. G., Dongre, A., Oppermann, U. C. T., & Athanasou, N. A. (2013) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-013-1399-z · Cited by 17
“A mutation in the gene coding DMP-1 results in autosomal recessive-inherited hypophosphataemic rickets [14, 15].”
BackgroundInherited disorders of calcium and phosphate metabolism
Gattineni, J. (2014) · Current Opinion in Pediatrics · doi:10.1097/mop.0000000000000064 · Cited by 18
Extracellular matrix protein DMP1 suppresses osteogenic differentiation of Mesenchymal Stem Cells
Zhang, S., Wan, H., Wang, P., Liu, M., Li, G., Zhang, C., & Sun, Y. (2018) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2018.05.092 · Cited by 17
Self-citationPrimary Disorders of Phosphate Metabolism
Carpenter, T. O. (2014) · Cited by 17
The Dentin Matrix Acidic Phosphoprotein 1 (DMP1) in the Light of Mammalian Evolution
Silvent, J., Sire, J., & Delgado, S. (2013) · Journal of Molecular Evolution · doi:10.1007/s00239-013-9539-2 · Cited by 17
“Therefore, we predict that the substitution of one of these conserved positions in human DMP1 would lead to either rickets or osteomalacia, and/or partial failure in predentin maturation (Ye 2004; Ye et al. 2005; Feng et al. 2006; Lorenz-Depiereux et al. 2006).”
BackgroundFemale-Specific Induction of Rat Pituitary Dentin Matrix Protein-1 by GnRH
Kučka, M., Bjelobaba, I. M., Clokie, S. J. H., Klein, D. C., & Stojilković, S. S. (2013) · Molecular Endocrinology · doi:10.1210/me.2013-1068 · Cited by 17
“Experiments with Dmp1 knockout mice have defective dentin development, hypomineralization, and rickets, confirming the importance of this protein in mineralization (49, 51).”
BackgroundChen, S., Olsen, K., Grigsby, C. L., & Gardner, D. G. (2007) · Kidney International · doi:10.1038/sj.ki.5002274 · Cited by 17
Clinical Disorders of Phosphate Homeostasis
Hansen, K. E., & Drezner, M. K. (2011) · Elsevier eBooks · doi:10.1016/b978-0-12-381978-9.10063-0 · Cited by 17
Self-citationInvolvement of the Klotho Protein in Dentin Formation and Mineralization
Suzuki, H., Amizuka, N., Oda, K., Noda, M., Ohshima, H., & Maeda, T. (2007) · The Anatomical Record · doi:10.1002/ar.20630 · Cited by 17
“Rescue of odontogenesis in Dmp1deficient mice by targeted re-expression of DMP1 reveals roles for DMP1 in early odontogenesis and dentin apposition in vivo.”
InfluentialJia, M., Chen, S., Zhang, B., Liang, H., Feng, J., & Zong, Z. (2013) · PLoS ONE · doi:10.1371/journal.pone.0074093 · Cited by 17
“Runx2 and BSP are markers for osteoblasts at the early and late stages, respectively [29,33].”
BackgroundMethodSelf-citationGlorieux, F. H., Bonewald, L. F., Harvey, N. C., & van der Meulen, M. C. H. (2022) · Orphanet Journal of Rare Diseases · doi:10.1186/s13023-021-02156-x · Cited by 16
“These proteins are expressed in late osteoblasts/early osteoid osteocytes while they are embedding in the osteoid matrix [81, 82].”
BackgroundSelf-citationFGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice
Courbon, G., Kentrup, D., Thomas, J. J., Wang, X., Tsai, H., Spindler, J. J., Drasek, J. C. V., Ndjonko, L. C. M., Martínez‐Calle, M., Lynch, E. P., et al. (2023) · JCI Insight · doi:10.1172/jci.insight.156850 · Cited by 18
“The convergence of phenotypes between XLH and ARHR (4, 5, 21, 22) suggests that humans and animals with ARHR might also benefit from FGF23 correction.”
BackgroundMethodInfluentialSelf-citationMechanistic insights into bone destruction in multiple myeloma: Cellular and molecular perspectives
Lungu, O., Toscani, D., & Giuliani, N. (2025) · Journal of bone oncology · doi:10.1016/j.jbo.2025.100668 · Cited by 21
“Osteocytes also produce fibroblast growth factor 23 (FGF23), an endocrine hormone that acts on the kidneys to decrease phosphate reabsorption and suppress vitamin D activation, thus playing a critical role in maintaining mineral balance [67].”
Rauner, M., Stein, N., & Hofbauer, L. C. (2011) · Springer eBooks · doi:10.1007/978-3-7091-0520-7_1 · Cited by 16
Exome sequencing reveals a mutation in DMP1 in a family with familial sclerosing bone dysplasia
Gannagé‐Yared, M., Makrythanasis, P., Chouery, É., Sobacchi, C., Mehawej, C., Santoni, F. A., Guipponi, M., Antonarakis, S. E., Hamamy, H., & Mégarbané, A. (2014) · Bone · doi:10.1016/j.bone.2014.08.014 · Cited by 16
“[4,5] with a final height ranging from 136 to 172 cm suggesting a great phenotypic variation.”
BackgroundInfluentialEffects of Rosiglitazone on the Outcome of Experimental Periapical Lesions in Mice
de Oliveira, K. M. H., Garlet, G. P., ROSSI, A. D., Barreiros, D., de Queiroz, A. M., da Silva, L. A. B., Nelson‐Filho, P., & da Silva, R. A. B. (2017) · Journal of Endodontics · doi:10.1016/j.joen.2017.06.026 · Cited by 16
“highly expressed in odontoblasts and osteoblasts/osteocytes (11).”
Dentin and Bone: Similar Collagenous Mineralized Tissues
MacDougall, M. J., & Javed, A. (2010) · Springer eBooks · doi:10.1007/978-1-84882-822-3_11 · Cited by 17
Platelet‐rich plasma enhances the differentiation of dental pulp progenitor cells into odontoblasts
Yeom, K.-W., Ariyoshi, W., Okinaga, T., Washio, A., Morotomi, T., Kitamura, C., & Nishihara, T. (2015) · International Endodontic Journal · doi:10.1111/iej.12443 · Cited by 16
“DMP-1 was originally identified in a cDNA library of rat incisor pulp (George et al. 1994), and found to play a crucial role in mineralized tissues formation (Ye et al. 2004, Ye et al. 2005, Feng et al. 2006).”
BackgroundMalaval, L., Aubin, J. E., & Vico, L. (2009) · Osteoporosis International · doi:10.1007/s00198-009-0869-2 · Cited by 23
“osteomalacia [15], at least in part indirectly, through impaired maturation of osteocytes, which are necessary to proper mineralization, and also increased levels of FGF-23 (a powerful negative regulator of phosphatemia [ 16 ]) as well as MEPE [17].”
BackgroundDental and Skeletal Applications of Silica-Based Nanomaterials
Ha, S., Weitzmann, M. N., & Beck, G. R. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4557-3127-5.00004-0 · Cited by 16
Schulze, J., Albers, J., Baranowsky, A., Keller, J., Spiro, A. S., Streichert, T., Zustin, J., Amling, M., & Schinke, T. (2009) · Bone · doi:10.1016/j.bone.2009.09.024 · Cited by 16
“bone formation and/or bone matrix mineralization [26–31].”
Uday, S., & Högler, W. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.65426-0 · Cited by 16
Li, Q., Philip, V. M., Stearns, T. M., Bubier, J. A., King, B. L., Low, B. E., Wiles, M. V., Saeidian, A. H., Sundberg, B. A., Uitto, J., et al. (2019) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2019.04.023 · Cited by 15
“Mutations in DMP1 cause autosomal recessive hypophosphatemia, a disease that manifests as rickets and osteomalacia, and when deleted in mice, results in a hypomineralized bone phenotype (Feng et al., 2006; Feng et al., 2003).”
BackgroundNi, X., Li, X., Zhang, Q., Liu, C., Gong, Y., Wang, O., Li, M., Xing, X., Jiang, Y., & Xia, W. (2020) · Calcified Tissue International · doi:10.1007/s00223-020-00755-7 · Cited by 16
“Hypophosphatemia resulted in highly expended growth plate and then led to short stature [3, 11].”
BackgroundInfluentialKonno, Y., Moore, R., Kamiya, N., & Negishi, M. (2009) · Pharmacogenetics and Genomics · doi:10.1097/fpc.0b013e328333bb28 · Cited by 15
Yajima, A., Tsuchiya, K., Burr, D. B., Minner, D. E., Condon, K. W., Miller, C. A., Satoh, S., Inaba, M., Nakayama, T., Tanizawa, T., et al. (2018) · Bone · doi:10.1016/j.bone.2018.05.002 · Cited by 15
Atkins, G. J., Findlay, D. M., Anderson, P., & Morris, H. A. (2011) · Elsevier eBooks · doi:10.1016/b978-0-12-381978-9.10023-x · Cited by 15
The Osteocyte Transcriptome: Discovering Messages Buried Within Bone
Wee, N. K. Y., Sims, N. A., & Morello, R. (2021) · Current Osteoporosis Reports · doi:10.1007/s11914-021-00708-5 · Cited by 15
He, Y., Wang, W., Ping, L., Wang, Y., He, Z., Dong, W., Jia, M., Yu, X., Yang, B., & Wang, J. (2022) · Bone · doi:10.1016/j.bone.2022.116522 · Cited by 15
Self-citationAramwit, P., Srisawadwong, R., & Supasyndh, O. (2011) · Journal of Nephrology · doi:10.5301/jn.5000011 · Cited by 15
Farahani, R. H., Nguyen, K.-A. T., Simonian, M. R., & Hunter, N. (2010) · American Journal Of Pathology · doi:10.2353/ajpath.2010.100073 · Cited by 15
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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