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Details for anatomical structure: osteoblast

EndoNet ID: ENC00093

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Synonyms

osteoblast, Gegenbaur`s cell, osteoplast, bone cell, skeletogenous cell, Osteoblastocytus

General information

They are responsible for the formation of the specialized interstitia matrix, the osteoid, and for the calzification of the osteoid into bone matrix

Links to other resources

Cytomer cy0052318

Larger structures

    Substructures

      Secreted hormones

      • Hormone: TGF-beta 2

        • In osteoblasts, TGF-beta 2 gene transcription is increased by 1alpha,25(OH)2D3. [1]
        • Osteoblasts expresses mRNA transcripts of TGF-beta1, TGF-beta2, TGF-beta 3, TGF-beta type I and type II receptors. [2]

        Influenced by:

        • VDR
          in osteoblast
      • Hormone: TGF-beta 1

        • Osteoblasts expresses mRNA transcripts of TGF-beta1, TGF-beta2, TGF-beta 3, TGF-beta type I and type II receptors. [2]
      • Hormone: TGF-beta 3

        • Osteoblasts expresses mRNA transcripts of TGF-beta1, TGF-beta2, TGF-beta 3, TGF-beta type I and type II receptors. [2]
      • Hormone: IL-11

        • IL-11 is produced by a variety of stromal cells including fibroblasts, epithelial cells and osteoblasts. [3]
        • IL-11 is an IL-6-type cytokine, which inhibits adipogenesis and activates osteoclasts. [4]

        Influenced by:

        • beta-2 adrenoreceptor
          in osteoblast
          • Interleukin-6 and interleukin-11 synthesis is stimulated by epinephrine in human osteoblasts. [4]
      • Hormone: C-C motif chemokine 2

        • OSM induces CCL-2 expression in osteoblasts. [5]
      • Hormone: IL-18

      • Hormone: BMP-3

      • Hormone: IGF-1

        • IGF-1 and IGF-2 are expressed by osteoblasts and act locally to stimulate both bone formation and resorption. [6]

        Influenced by:

        • AR
          in osteoblast
          • The nonaromatizable androgen, 5alpha-dihydrotestosterone (5alphaDHT), and testosterone, but not dehydroepiandrosterone, increased IGF-I messenger RNA (mRNA) levels up to 4-fold in a dose (10(-12)-10(-6) M)- and time (2-72 h)-dependent fashion. [7]
        • ER-alpha
          in osteoblast
          • Human fetal osteoblast cells (hFOB/ER9) with E2 increased steady state levels of IGF-I mRNA in a time- and dose- dependent fashion with a maximal increase of 319% +/- 33% (P < 0.01) of control occurring after treatment with 10(-7) M E2 for 48 hours. [8]
        • ER-beta
          in osteoblast
          • Human fetal osteoblast cells (hFOB/ER9) with E2 increased steady state levels of IGF-I mRNA in a time- and dose- dependent fashion with a maximal increase of 319% +/- 33% (P < 0.01) of control occurring after treatment with 10(-7) M E2 for 48 hours. [8]
      • Hormone: RANKL

        • PTH and VD3 (calcitriol) increase the expression of RANKL on the surface of osteoblasts and bone marrow stem cells. [6]

        Influenced by:

        • VDR
          in osteoblast
        • PTHR1
          in osteoblast
      • Hormone: interleukin 6

        • Sex hormones suppress the synthesis and secretion of IL-6 by osteoblasts and bone marrow stem cells. [6]
        • IL-6 is a potent regulator for osteoclast differentiation and elicits bone resorption in in vivo and in vitro models that contain early osteoclast precursors. [4]
        • IL-6 and IL-11, synthesized in osteoblasts, are important stimulators of osteoclast development and physiologically regulate bone metabolism. [4]

        Influenced by:

        • PTHR1
          in osteoblast
          • Il-6 is produced by osteoblasts, and its production is stimulated by PTH and PGE2. [9]
        • EP3
          in osteoblast
          • Il-6 is produced by osteoblasts, and its production is stimulated by PTH and PGE2. [9]
        • EP4
          in osteoblast
          • Il-6 is produced by osteoblasts, and its production is stimulated by PTH and PGE2. [9]
        • IL-4Ralpha
          in osteoblast
          • Receptor-blocking antibodies to IL-4Ralpha inhibited the induction of IL-6 formation by both IL-4 and IL-13. IL-4 was tenfold more potent than IL-13 in inducing both alkaline phosphatase (ALP) activity and IL-6 secretion, whereas the cytokines were equipotent as inhibitors of cell proliferation. [10]
        • beta-2 adrenoreceptor
          in osteoblast
          • The maximum level of IL-6 production was over 40 pg/mL after 6 hr. The maximum level of IL-6 production was obtained at 10–100 &#x3bc;M epinephrine. [4]
        • bradykinin receptor B2
          in osteoblast
          • Bradykinin increased the synthesis of both IL-6 and PGE(2) and the increase in both was blocked by HOE140 (B2R antagonist). [11]
          • Bradykinin increased IL-6 and PGE2 synthesis via B2R but not B1R. [11]
      • Hormone: M-CSF

        • In vivo, CSF-1 synthesis by osteoblasts is temporally and spatially related to sites of osteoclast development. [12]

        Influenced by:

        • PTHR1
          in osteoblast
          • Stromal cells and osteoblasts express RANKL and M-CSF, which are up-regulated by osteoclastogenic molecules such as PTH. [13]
      • Hormone: IGFBP-4

        Influenced by:

        • AR
          in osteoblast
          • 5-alpha-DHT decreased IGFBP-4 mRNA and protein levels by 2- and 4-fold. [7]
        • ER-alpha
          in osteoblast
          • Treatment with E2 at 0.01-10 nM for 48 h increased IGFBP-4 mRNA to 346% +/- 90% (mean +/- SE) of control (p < 0.05) and IGFBP-4 protein to 278% +/- 75% of control (p < 0.01) in a dose-dependent fashion. [8]
        • ER-beta
          in osteoblast
          • Treatment with E2 at 0.01-10 nM for 48 h increased IGFBP-4 mRNA to 346% +/- 90% (mean +/- SE) of control (p < 0.05) and IGFBP-4 protein to 278% +/- 75% of control (p < 0.01) in a dose-dependent fashion [8]
      • Hormone: IGFBP-2

        Influenced by:

        • AR
          in osteoblast
          • 5-alpha-DHT increased IGFBP-2 and -3 mRNA and protein levels by 6- and 7-fold (for mRNA) and 3- and 5-fold (for protein). [7]
      • Hormone: IGFBP-3

        Influenced by:

        • AR
          in osteoblast
          • 5-alpha-DHT increased IGFBP-2 and -3 mRNA and protein levels by 6- and 7-fold (for mRNA) and 3- and 5-fold (for protein). [7]
      • Hormone: PGE2

        Influenced by:

        • IL-4Ralpha
          in osteoblast
        • bradykinin receptor B2
          in osteoblast
          • Bradykinin increased the synthesis of both IL-6 and PGE(2) and the increase in both was blocked by HOE140 (B2R antagonist). [11]
          • [11]
        • bradykinin receptor B1
          in osteoblast
          • The B2 receptors are linked to a burst of prostanoid release, whereas the B1 receptors mediate a delayed prostaglandin response [14]
      • Hormone: amphiregulin

        • Amphiregulin (AR) is a potent growth factor for the preosteoblast but it also strongly inhibits osteoblast differentiation. [15]

        Influenced by:

        • PTHR1
          in osteoblast
          • PTH rapidly and strongly stimulates the expression of amphiregulin not only in several osteoblastic cell lines but also in bone. [15]
        • EP3
          in osteoblast
          • In addition to PTH, PGE2 also strongly stimulates AR expression through the CREB phosphorylation pathway. [15]
        • EP4
          in osteoblast
          • In addition to PTH, PGE2 also strongly stimulates AR expression through the CREB phosphorylation pathway. [15]
      • Hormone: osteopontin

      • Hormone: osteonectin

      • Hormone: vitronectin

      • Hormone: osteocalcin

      • Hormone: decorin

      • Hormone: thrombospondin 1

      • Hormone: IL-1 alpha

      • Hormone: IL-1 beta

      • Hormone: IL-11

      • Hormone: CNTF

      • Hormone: TNF-alpha

      • Hormone: LIF

      • Hormone: M-CSF

      • Hormone: oncostatin M

      • Hormone: VEGF-165

      • Hormone: IAPP

      • Hormone: cardiotrophin 1

      • Hormone: osteomodulin

      • Hormone: bone sialoprotein 2

      • Hormone: IGF

      • Hormone: Dkk1

      • Hormone: sFRP-2

      • Hormone: sclerostin

      • Hormone: sclerostin

      • Hormone: noggin

      • Hormone: gremlin-2

      • Hormone: Wnt-1

      • Hormone: Wnt-4

      • Hormone: WNT9A

      • Hormone: Wnt-7b

        • Wnt7b is produced by osteoblasts. [16]
      • Hormone: WISP-2

      • Hormone: chordin-like protein 2

      • Hormone: EGF

      • Hormone: IGF-2

        • IGF-1 and IGF-2 are expressed by osteoblasts and act locally to stimulate both bone formation and resorption. [6]
      • Hormone: PGI2

        Influenced by:

        • bradykinin receptor B2
          in osteoblast
          • The B2 receptors are linked to a burst of prostanoid release. [14]
        • bradykinin receptor B1
          in osteoblast

      Receptors

      • Receptor: ER-alpha

        Induced phenotype:

        • antiapoptotic effect
          • The membrane localization of ER alpha and its interaction with caveolin-1 are required for stretching-induced external signal-regulated kinases (ERKs) activation and anti-apoptosis in osteocytes and osteoblasts. [17]

        Influences:

        • IGF-1
          • Human fetal osteoblast cells (hFOB/ER9) with E2 increased steady state levels of IGF-I mRNA in a time- and dose- dependent fashion with a maximal increase of 319% +/- 33% (P < 0.01) of control occurring after treatment with 10(-7) M E2 for 48 hours. [8]
        • IGFBP-4
          • Treatment with E2 at 0.01-10 nM for 48 h increased IGFBP-4 mRNA to 346% +/- 90% (mean +/- SE) of control (p < 0.05) and IGFBP-4 protein to 278% +/- 75% of control (p < 0.01) in a dose-dependent fashion. [8]
      • Receptor: ER-beta

        Influences:

        • IGF-1
          • Human fetal osteoblast cells (hFOB/ER9) with E2 increased steady state levels of IGF-I mRNA in a time- and dose- dependent fashion with a maximal increase of 319% +/- 33% (P < 0.01) of control occurring after treatment with 10(-7) M E2 for 48 hours. [8]
        • IGFBP-4
          • Treatment with E2 at 0.01-10 nM for 48 h increased IGFBP-4 mRNA to 346% +/- 90% (mean +/- SE) of control (p < 0.05) and IGFBP-4 protein to 278% +/- 75% of control (p < 0.01) in a dose-dependent fashion [8]
      • Receptor: AR

        Influences:

        • IGF-1
          • The nonaromatizable androgen, 5alpha-dihydrotestosterone (5alphaDHT), and testosterone, but not dehydroepiandrosterone, increased IGF-I messenger RNA (mRNA) levels up to 4-fold in a dose (10(-12)-10(-6) M)- and time (2-72 h)-dependent fashion. [7]
        • IGFBP-4
          • 5-alpha-DHT decreased IGFBP-4 mRNA and protein levels by 2- and 4-fold. [7]
        • IGFBP-2
          • 5-alpha-DHT increased IGFBP-2 and -3 mRNA and protein levels by 6- and 7-fold (for mRNA) and 3- and 5-fold (for protein). [7]
        • IGFBP-3
          • 5-alpha-DHT increased IGFBP-2 and -3 mRNA and protein levels by 6- and 7-fold (for mRNA) and 3- and 5-fold (for protein). [7]
      • Receptor: IL-1RI

      • Receptor: VDR

        Induced phenotype:

        • regulation of gene expression
          • After binding of calcitriol vitamin D receptor regulates gene transcription by binding to vitamin D responsive elements in promotor region of target genes. [18]
        • alopecia
          • Functional inactivation of vitamin D receptor results in alopecia. [18]
        • mineral metabolism
          • Calcitriol, the biologically active form of vitamin D, is essential for intact mineral metabolism,has important roles in calcium and phosphate homeostasis and in the regulation of cell proliferation and differentiation. [19]
        • rickets
          • Functional inactivation of vitamin D receptor results in rickets. [18]

        Influences:

        • TGF-beta 2
        • RANKL
        • FGF-23
          • The bone, likely the osteoblast or its precursor cell, is a major source of FGF23 in response to 1alpha,25-Dihydroxyvitamin D3. [20]
          • 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. [20]
          • 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. [20]
      • Receptor: TGF-beta type II receptor

      • Receptor: TGF-beta type I receptor

      • Receptor: PTHR1

        Influences:

        • RANKL
        • M-CSF
          • Stromal cells and osteoblasts express RANKL and M-CSF, which are up-regulated by osteoclastogenic molecules such as PTH. [13]
        • interleukin 6
          • Il-6 is produced by osteoblasts, and its production is stimulated by PTH and PGE2. [9]
        • amphiregulin
          • PTH rapidly and strongly stimulates the expression of amphiregulin not only in several osteoblastic cell lines but also in bone. [15]
      • Receptor: EP3

        Influences:

        • interleukin 6
          • Il-6 is produced by osteoblasts, and its production is stimulated by PTH and PGE2. [9]
        • amphiregulin
          • In addition to PTH, PGE2 also strongly stimulates AR expression through the CREB phosphorylation pathway. [15]
      • Receptor: EP4

        Influences:

        • interleukin 6
          • Il-6 is produced by osteoblasts, and its production is stimulated by PTH and PGE2. [9]
        • amphiregulin
          • In addition to PTH, PGE2 also strongly stimulates AR expression through the CREB phosphorylation pathway. [15]
      • Receptor: IGF-1R

      • Receptor: IL-13Ralpha

      • Receptor: IL-4Ralpha

        Influences:

        • interleukin 6
          • Receptor-blocking antibodies to IL-4Ralpha inhibited the induction of IL-6 formation by both IL-4 and IL-13. IL-4 was tenfold more potent than IL-13 in inducing both alkaline phosphatase (ALP) activity and IL-6 secretion, whereas the cytokines were equipotent as inhibitors of cell proliferation. [10]
        • PGE2
      • Receptor: beta-2 adrenoreceptor

        Influences:

        • interleukin 6
          • The maximum level of IL-6 production was over 40 pg/mL after 6 hr. The maximum level of IL-6 production was obtained at 10–100 &#x3bc;M epinephrine. [4]
        • IL-11
          • Interleukin-6 and interleukin-11 synthesis is stimulated by epinephrine in human osteoblasts. [4]
      • Receptor: calcitonin-receptor-like receptor

      • Receptor: VPAC1

        • VPAC1 receptors are expressed in human osteoblasts. [21]

        Induced phenotype:

        • negative regulation of bone resorption
          • PACAP has been found to inhibit bone resorption by rabbit osteoblasts. [22]
      • Receptor: NPY1-R

      • Receptor: bradykinin receptor B2

        Influences:

        • interleukin 6
          • Bradykinin increased the synthesis of both IL-6 and PGE(2) and the increase in both was blocked by HOE140 (B2R antagonist). [11]
          • Bradykinin increased IL-6 and PGE2 synthesis via B2R but not B1R. [11]
        • PGE2
          • Bradykinin increased the synthesis of both IL-6 and PGE(2) and the increase in both was blocked by HOE140 (B2R antagonist). [11]
          • [11]
        • PGI2
          • The B2 receptors are linked to a burst of prostanoid release. [14]
      • Receptor: bradykinin receptor B1

        • The angiogenic effect of BK is due to the direct activation of B1 receptor on capillary endothelial cells, which transduces the autocrine up-regulation of FGF-2 by the endogenous activation of the NOS pathway. [23]

        Influences:

        • PGE2
          • The B2 receptors are linked to a burst of prostanoid release, whereas the B1 receptors mediate a delayed prostaglandin response [14]
        • PGI2
      • Receptor: OPG

      • Receptor: LRP5

      • Receptor: kremen 1

      • Receptor: THRA1

      • Receptor: THRB1

      • Receptor: thyroid hormone receptor alpha2

      • Receptor: thyroid hormone receptor beta 2

      • Receptor: Tumor necrosis factor receptor superfamily member 11B

        Induced phenotype:

        • negative regulation of osteoclast differentiation
          • Tumor necrosis factor receptor superfamily member 11B specifically inhibits osteoclastogenesis in a dose-dependent manner elicited through three distinct signaling patways stimulated by 1alpha,25-dihydroxy vitamin D3, parathyroid hormone, and interleukin-11. [24]
        • Paget disease, juvenlie
          • Juvenile Paget disease can result from osteoprotegerin deficiency by homozygous or compound heterozygous mutation in the TNFRSF11B gene. [25]
      • Receptor: PRLR

      • Receptor: Sphingosine 1-phosphate receptor 2

        Induced phenotype:

        • positive regulation of osteoblast proliferation
          • S1P is a potent osteoblast mitogen in vitro, exerting its proliferative effects in part via a signaling pathway that involves edg5. [26]
      • Receptor: Sphingosine 1-phosphate receptor 1

      • Receptor: Sphingosine 1-phosphate receptor 5

      • Receptor: Lysophosphatidic acid receptor 1

        Induced phenotype:

        • skeletal system development
          • The finding of craniofacial deformities in mice in which the gene for edg-2 has been deleted suggests that phospholipids may participate in skeletal development. [27]
      Reference