ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2016
Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pi t1 Double-Knockout Mice.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 63 citations in OpenAlex.
- Phosphate homeostasis and endocrine regulators.Pediatric nephrology (Berlin, Germany) · 2026Review
- TNAP and PHOSPHO1 Function Synergistically to Afford Critical Control Over the Mineralization of the Postnatal Murine Skeleton.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanobiology of hypertrophic chondrocyte mineralization: Biomechanical regulation and therapeutic implications in skeletal disorders.Mechanobiology in medicine · 2026Review
- TNAP and PHOSPHO1 function synergistically to afford critical control over the mineralisation of the postnatal murine skeleton.bioRxiv : the preprint server for biology · 2026Article
- Modulation of TNAP activity and apatite formation in biomimetic matrix vesicles studied byBiochimica et biophysica acta. Biomembranes · 2025Article
- Osteoblasts sense extracellular levels of phosphate to control the local expression of phosphatases for matrix mineralisation.Bone reports · 2025Article
- Taking a closer look at matrix vesicle biogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Review
- DSP and DPP are dispensable for initiation of dentin and enamel mineralization but critical for circumpulpal dentin mineralization.Scientific reports · 2025Article
- Phosphate in Physiological and Pathological Mineralization: Important yet Often Unheeded.MedComm · 2025Review
- Do Media Extracellular Vesicles and Extracellular Vesicles Bound to the Extracellular Matrix Represent Distinct Types of Vesicles?Biomolecules · 2023Review
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- NPP1 and TNAP hydrolyze ATP synergistically during biomineralization.Purinergic signalling · 2023Article
- Spatial Lipidomic Profiling of Mouse Joint Tissue Demonstrates the Essential Role of PHOSPHO1 in Growth Plate Homeostasis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Gene Therapy Using Recombinant AAV Type 8 Vector Encoding TNAP-DJBMR plus · 2023Article
- Shedding Light on the Role of Na,K-ATPase as a Phosphatase during Matrix-Vesicle-Mediated Mineralization.International journal of molecular sciences · 2022Article
- Mineralization Profile of Annexin A6-Harbouring Proteoliposomes: Shedding Light on the Role of Annexin A6 on Matrix Vesicle-Mediated Mineralization.International journal of molecular sciences · 2022Article
- Proton Pump Inhibitors Inhibit PHOSPHO1 Activity and Matrix Mineralisation In Vitro.Calcified tissue international · 2021Article
- The Physiological and Pathological Role of Tissue Nonspecific Alkaline Phosphatase beyond Mineralization.Biomolecules · 2021Review
- Rickets in Children: An Update.Biomedicines · 2021Review
- Hormonal regulation of biomineralization.Nature reviews. Endocrinology · 2021Review
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11 authors at 7 institutions in 5 countries.
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Abstract
We have previously shown that ablation of either the Phospho1 or Alpl gene, encoding PHOSPHO1 and tissue-nonspecific alkaline phosphatase (TNAP) respectively, lead to hyperosteoidosis, but that their chondrocyte-derived and osteoblast-derived matrix vesicles (MVs) are able to initiate mineralization. In contrast, the double ablation of Phospho1 and Alpl completely abolish initiation and progression of skeletal mineralization. We argued that MVs initiate mineralization by a dual mechanism: PHOSPHO1-mediated intravesicular generation of inorganic phosphate (Pi ) and phosphate transporter-mediated influx of Pi . To test this hypothesis, we generated mice with col2a1-driven Cre-mediated ablation of Slc20a1, hereafter referred to as Pi t1, alone or in combination with a Phospho1 gene deletion. Pi t1(col2/col2) mice did not show any major phenotypic abnormalities, whereas severe skeletal deformities were observed in the [Phospho1(-/-) ; Pi t1(col2/col2) ] double knockout mice that were more pronounced than those observed in the Phospho1(-/-) mice. Histological analysis of [Phospho1(-/-) ; Pi t1(col2/col2) ] bones showed growth plate abnormalities with a shorter hypertrophic chondrocyte zone and extensive hyperosteoidosis. The [Phospho1(-/-) ; Pi t1(col2/col2) ] skeleton displayed significant decreases in BV/TV%, trabecular number, and bone mineral density, as well as decreased stiffness, decreased strength, and increased postyield deflection compared to Phospho1(-/-) mice. Using atomic force microscopy we found that ∼80% of [Phospho1(-/-) ; Pi t1(col2/col2) ] MVs were devoid of mineral in comparison to ∼50% for the Phospho1(-/-) MVs and ∼25% for the WT and Pi t1(col2/col2) MVs. We also found a significant decrease in the number of MVs produced by both Phospho1(-/-) and [Phospho1(-/-) ; Pi t1(col2/col2) ] chondrocytes. These data support the involvement of phosphate transporter 1, hereafter referred to as Pi T-1, in the initiation of skeletal mineralization and provide compelling evidence that PHOSPHO1 function is involved in MV biogenesis. © 2016 American Society for Bone and Mineral Research.
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