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Matrix Extracellular Phosphoglycoprotein (MEPE) Is a New Bone Renal Hormone and Vascularization Modulator
Open accessAbstract
Increased matrix extracellular phosphoglycoprotein (MEPE) expression occurs in several phosphate and bone-mineral metabolic disorders. To resolve whether MEPE plays a role, we created a murine model overexpressing MEPE protein (MEPE tgn) in bone. MEPE tgn mice displayed a growth and mineralization defect with altered bone-renal vascularization that persisted to adulthood. The growth mineralization defect was due to a decrease in bone remodeling, and MEPE tgn mice were resistant to diet-induced renal calcification. MEPE protein-derived urinary ASARM peptides and reduced urinary Ca X PO4 product mediated the suppressed renal calcification. Osteoblastic cells displayed reduced activity but normal differentiation. Osteoclastic precursors were unable to differentiate in the presence of osteoblasts. In the kidney, NPT2a up-regulation induced an increase in phosphate renal reabsorption, leading to hyperphosphatemia. We conclude MEPE and MEPE-phosphate-regulating gene with homologies to endopeptidases on the X chromosome (MEPE-PHEX) interactions are components to an age-diet-dependent pathway that regulates bone turnover and mineralization and suppresses renal calcification. This novel pathway also modulates bone-renal vascularization and bone turnover.
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“A study demonstrated that transgenic mice overexpressing MEPE exhibited reduced renal calcification despite hyperphosphatemia 46 .”
From Sex-specific gene expression signatures of calcific aortic valve stenosis in a large collection of human tissues (2026) · cites this paper as [46]
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MEPE, a New Gene Expressed in Bone Marrow and Tumors Causing Osteomalacia
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Self-citationAldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity
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MEPE has the properties of an osteoblastic phosphatonin and minhibin
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Research works printed but not linked: 2
- Yang, 2006, MEPE over-expression in osteocytes of Dmp1 null mice by activation of the PKA/CREB pathway, J Bone Miner Res, 21, S136
- Martin, 2008, MEPE C-terminal ASARM-peptide promotes hypophosphatemia, bone defects and increases adiposity, J Bone Miner Res, 23, S103
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Metadata
- Authors
- David, V., Martin, A., Hedge, A.-M., & Rowe, P. S. N.
- Affiliations
- University of Kansas Medical Center (US)
- Corresponding author
- Rowe, Peter S. N.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2009-09-01
- Volume
- 150
- Issue
- 9
- Pages
- 4012-4023
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC2819738
- OpenAlex
- W2000443667
- Cited by
- 106
- References
- 50
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 7 · 2021: 3 · 2020: 9 · 2019: 5 · 2018: 6 · 2017: 2 · 2016: 5 · 2015: 10 · 2014: 3 · 2013: 15 · 2012: 9
- FWCI
- 6.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ar051598-09)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01-AR051598)
- 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
- MEPE, bone mineralization, bone remodeling, renal calcification, phosphate metabolism, hyperphosphatemia, Npt2a, osteogenic differentiation, osteoclastogenesis, bone turnover
- MeSH terms
- Aging, Aldosterone, Animals, Animal Nutritional Physiological Phenomena, Bone and Bones, Bone Development, Calcitriol, Glycoproteins, Hypocalcemia, Kidney, Mice, Inbred C57BL, Mice, Transgenic, Neovascularization, Pathologic, Parathyroid Hormone, Phosphoproteins, Extracellular Matrix Proteins, Vascular Endothelial Growth Factor A, Mice, PHEX Phosphate Regulating Neutral Endopeptidase, Osteopontin, Hyperphosphatemia
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