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Details for anatomical structure: bone

EndoNet ID: ENC00382

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Synonyms

bone, , Os

General information

Hard connective tissue consisting of cells embedded in a matrix of mineralized ground substance and collagen fibers, the fibers are impregnated with a form of calcium phosphate similar to hydroxyapatite as well as with substantial quantities of carbonate, citrate sodium, and magnesium; bone is composed of 75% inorganic material and 25% organic material; bone consists of a dense outer layer of compact substance or cortical substance covered by the periosteum, and an inner loose, spongy substance; the central portion of a long bone is filled with marrow

Links to other resources

Cytomer cy0052290

Larger structures

    Substructures

      Secreted hormones

      • Hormone: sclerostin

      • Hormone: Spp-24

      • Hormone: FGF-23

        • FGF23 mRNA expression is found to be highest in bone in both the human and the mouse. [1]

        Influenced by:

        • VDR
          in bone
          • The bone, likely the osteoblast or its precursor cell, is a major source of FGF23 in response to 1alpha,25-Dihydroxyvitamin D3. [1]
          • This establishes a reciprocal relationship between 1,25(OH)2D3 and FGF23, with phosphatemic 1,25(OH)2D3 hormone generated in the kidney, inducing skeletal endocrine cells to produce FGF23, which then feedback represses renal 1alpha-OHase to curtail 1,25(OH)2D3 biosynthesis as well as inhibits the renal reabsorption of phosphate to elicit phosphaturia. [1]
          • 1,25(OH)2D3-induced FGF23 from bone constitutes the final link in a renal-gastrointestinal-skeletal axis that controls serum phosphate and active vitamin D levels. [1]
        • VDR
          in osteoblast
          • The bone, likely the osteoblast or its precursor cell, is a major source of FGF23 in response to 1alpha,25-Dihydroxyvitamin D3. [1]
          • This establishes a reciprocal relationship between 1,25(OH)2D3 and FGF23, with phosphatemic 1,25(OH)2D3 hormone generated in the kidney, inducing skeletal endocrine cells to produce FGF23, which then feedback represses renal 1alpha-OHase to curtail 1,25(OH)2D3 biosynthesis as well as inhibits the renal reabsorption of phosphate to elicit phosphaturia. [1]
          • 1,25(OH)2D3-induced FGF23 from bone constitutes the final link in a renal-gastrointestinal-skeletal axis that controls serum phosphate and active vitamin D levels. [1]

      Receptors

      • Receptor: VDR

        Induced phenotype:

        • tumor-induced osteomalacia
          • Ectopic overproduction of FGF23 overwhelms its processing and degradation, leading to TIO. [2]
          • Administration of recombinant FGF23 in normal and parathyroidectomized animals induced a decrease in serum phosphate levels, phosphaturia accompanied by a reduction in renal mRNA and protein levels for sodium-phosphate cotransport activites in the kidney, a decrease in renal mRNA for 25-hydroxyvitamin D-1{alpha}-hydroxylase, and an increase in 25-hydroxyvitamin D-24-hydroxylase, the cytochrome P-450 enzymes that generate and inactivate 1,25(OH)2D3 hormone, respectively [2]
          • Mice implanted with FGF23-expressing Chinese hamster ovary (CHO) cells showed more severe hypophosphatemia, osteomalacia, and decreased 1,25(OH)2D3 levels. [2]
        • autosomal dominant hypophosphatemic rickets
          • Missense mutations in FGF23, which likely prevent its cleavage and inactivation, are the cause of ADHR. [3]
          • Administration of an ADHR mutant form of FGF23 to mice inhibited sodium-phosphate cotransport activities in both the kidney and small intestine, and suppressed 1,25(OH)2D3. [4]
        • X-linked hypophosphatemic rickets
          • Elevated circulating FGF23 levels have been found in most, but not all, patients with XLH. [5]
        • osteoporosis
          • The primary form of circulating vitamin D, 25-hydroxy-vitamin D, is a modifiable quantitative trait associated with multiple medical outcomes, including osteoporosis. [6]

        Influences:

        • FGF-23
          • The bone, likely the osteoblast or its precursor cell, is a major source of FGF23 in response to 1alpha,25-Dihydroxyvitamin D3. [1]
          • This establishes a reciprocal relationship between 1,25(OH)2D3 and FGF23, with phosphatemic 1,25(OH)2D3 hormone generated in the kidney, inducing skeletal endocrine cells to produce FGF23, which then feedback represses renal 1alpha-OHase to curtail 1,25(OH)2D3 biosynthesis as well as inhibits the renal reabsorption of phosphate to elicit phosphaturia. [1]
          • 1,25(OH)2D3-induced FGF23 from bone constitutes the final link in a renal-gastrointestinal-skeletal axis that controls serum phosphate and active vitamin D levels. [1]
      • Receptor: PRLR

      • Receptor: Ovarian cancer G-protein coupled receptor 1

      Reference