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  • 1
    Electronic Resource
    Electronic Resource
    Properties of osteoblast-like cells isolated from the cortical endosteal bone surface of adult rabbits (1983)
    Springer
    Calcified tissue international 35 (1983), S. 571-577 
    Details
    ISSN: 1432-0827
    Keywords: Adult rabbits ; Endosteal bone cells ; Alkaline phosphatase ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The purpose of the present study was to isolate cells from the cortical endosteal bone surface of adult rabbits and characterize some properties of these cells in vitro. Following removal of the marrow from the medullary cavity of long bones, the cells lining the cortical endosteal bone surface were obtained by enzymatic digestion using 0.1% crude collagenase. These cells were examined immediately after isolation or following their growth for 8–10 days in primary culture. Freshly isolated cells contained 7–10 times more alkaline phosphatase (AP) than acid phosphatase activity. This AP activity was extremely heat labile (incubation at 58°C caused 〉90% loss of enzyme activity within 15 min) and significantly more sensitive to inhibition by levamisole and L-homoarginine than L-phenylalanine. Synthetic bPTH-(1–34) [1–100 ng/ml], native bPTH-(1–84) [1 U/ml] and prostaglandin E2 [1–10 µg/ml] all caused a significant accumulation of cAMP in cultured endosteal bone cells. In contrast, neither salmon calcitonin (1 U/ml) nor porcine insulin (10–1000 ng/ml) stimulated an increase in cAMP. These results suggest that cells isolated from the cortical endosteal bone surface of adult rabbits are osteoblasts or osteoblast-like. These cells retain their ability to respond in a specific manner to bone-seeking hormones following their growth in culture. Cortical endosteal bone cells isolated from rabbits of different ages, physiologic or pathologic conditions can be used to assess the changes in bone cell function and responsiveness which may accompany senescence or development of adult metabolic bone disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405096
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  • 2
    Electronic Resource
    Electronic Resource
    Response of periodontal ligament cells to orthodontic force: Ultrastructural identification of proliferating fibroblastsThis research was supported by the National Institute of Dental Research, NIH Research Grant DE 04371. (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 194 (1979), S. 603-613 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The morphologic response of periodontal ligament (PDL) cells in an area of tension created by orthodontic force has been assessed by transmission electron microscopy. Young adult male rats were sacrificed at 24, 48, 72, 96 and 120 hours following orthodontic stimulation. The earliest detectable response was the appearance of increased numbers of mitotic cells in the PDL at 24 hours post-stimulation. The most significant ultrastructural feature of these cells was the presence of intracellular vesicles containing collagen microfibrils. These vesicles were identical to profiles present in interphase PDL fibroblasts involved in collagen phagocytosis associated with turnover of the ligament. Between 48 and 120 hours the alveolar bone surface in the region examined was characterized by the presence of newly generated osteoblasts and active bone formation. Intracellular collagen was never observed in osteoblasts. These observations suggest that at least a portion of the population of PDL cells which proliferate in response to orthodontic force represent functional ligament fibroblasts.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091940412
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  • 3
    Electronic Resource
    Electronic Resource
    Plasminogen-dependent activation of latent transforming growth factor beta (TGFβ) by growing cultures of osteoblast-like cells (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 157 (1993), S. 528-534 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Osteoblasts secrete transforming growth factor beta (TGFβ) as a biologically inert, latent complex that must be dissociated before the growth factor can exert its effects. We have examined the production and proteolytic activation of latent TGFβ (LTGFβ) by clonal UMR 106-01 rat osteosarcoma cells and neonatal mouse calvarial (MC) osteoblast-like cells in vitro. Synthetic bPTH-(1-34) increased the activity of tissue-type (tPA) and urokinase-type (uPA) plasminogen activators (PA) in cell lysates (CL) of UMR 106-01 cells. The concentration of active TGFβ in serum-free CM from cultures treated with bPTH-(1-34) and plasminogen was significantly greater than in CM from untreated controls and cultures treated with either bPTH-(1-34) or plasminogen alone. This effect occurred at concentrations of PTH-(1-34) that increased PA activity and was prevented by aprotinin, an inhibitor of plasmin activity. Treatment with bPTH-(1-34) had no effect on the concentration of TGFβ in acid-activated samples of CM. Functional consequences of proteolytically activated TGFβ was examined in primary cultures of neonatal MC osteoblast-like cells. Human platelet TGFβ1 caused a dose-dependent increase in the migration of these cells in an in vitro wound healing assay. Cell migration was also stimulated in cultures treated with bPTH-(1-34) and plasminogen together. This effect was blocked by an anti-TGFβ1 antibody. The results of these studies demonstrate that (1) LTGFβ secreted by osteoblasts in vitro is activated under conditions where the plasmin activity in the cultures is increased, and (2) the TGFβ generated by plasmin-mediated proteolysis is biologically active. We suggest that the local concentration of TGFβ in bone may be controlled by the osteoblast-associated plasminogen activator/plasmin system. Furthermore, since several calciotropic factors influence osteoblast PA activity, this system may have an important role in mediating their anabolic and/or catabolic effects. © 1993 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041570312
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  • 4
    Electronic Resource
    Electronic Resource
    Plasminogen activator regulation in osteoblasts: Parathyroid hormone inhibition of type-1 plasminogen activator inhibitor and its mRNA (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 152 (1992), S. 346-355 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In order to determine the mechanism by which parathyroid hormone (PTH) stimulates plasminogen activator (PA) activity in rat osteoblasts, we investigated the effect of human PTH(1-34) [hPTH(1-34)] on the synthesis of mRNAs for tissue-type PA (tPA), urokinase-type PA (uPA), and PA inhibitor-1 (PAI-1), and on release of PA activity and PAI-1 protein in both normal rat calvarial osteoblasts and UMR 106-01 osteogenic sarcoma cells. hPTH(1-34) (0.25-25 nM) decreased PAI-1 mRNA and protein, and increased PA activity in both cell types in a dose-dependent manner with ED50 of about 1 nM for both responses. Forskolin and isobutylmethylxanthine also stimulated PA activity and decreased PAI-1 protein and mRNA in both cell types. hPTH(1-34) did not show any consistent effect on tPA and uPA mRNA in calvarial osteoblasts, but a modest (two-fold) increase of both mRNAs was observed in UMR 106-01 cells treated with 25 nM hPTH(1-34). However, when protein synthesis was inhibited with 100 μM cycloheximide, the increase of tPA and uPA mRNA by hPTH(1-34) was enhanced in UMR 106-01 cells and became evident in calvarial osteoblasts. Fibrin autography also revealed that hPTH(1-34) increases tPA and uPA activity, especially after cycloheximide treatment in UMR 106-01 cells. These results strongly suggest that PTH increases PA activity predominantly by decreasing PAI-1 protein production through a cyclic adenosine monophosphate (cAMP)-dependent mechanism in rat osteoblasts. The reduction of PAI-1 protein by PTH results in enhanced action of both tPA and uPA, and would contribute to the specific roles of these PAs in bone. © 1992 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041520216
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  • 5
    Electronic Resource
    Electronic Resource
    Parathyroid hormone stimulation of alkaline phosphatase activity in cultured neonatal mouse calvarial bone cells: Involvement of cyclic AMP and calcium (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 128 (1986), S. 246-250 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The involvement of cAMP and calcium in the rise in alkaline phosphatase (AP) activity observed when confluent, serum-free primary cultures of neonatal mouse calvarial cells are treated with parathyroid hormone (PTH) has been studied. Synthetic bovine PTH [bPTH-(1-34)] increased cellular cAMP at concentrations (10-9 to 10-7 M) previously found to elevate AP activity. Other substances that increase cAMP in these cells (forskolin, prostaglandin E2, 8-bromoadenosine cAMP and 3-isobutyl-1-methylxanthine) also increased enzyme activity. By comparison, increasing the concentration of calcium in the culture medium from 1.8 to 3.8 or 5.8 mM lowered the magnitude of the maximal AP response. In addition, treatment of cultures with the divalent cation ionophore A23187 caused a significant decrease in AP activity. These results suggest that: (1) cAMP mediates the rise in the specific activity of AP in cultured neonatal mouse calvarial cells treated with bPTH-(1-34) and (2) the concentration of calcium in the environment significantly influences the responsivity of bone cells to the hormone.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041280216
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  • 6
    Electronic Resource
    Electronic Resource
    Transforming growth factor beta inhibits plasminogen activator (PA) activity and stimulates production of urokinase-type PA, PA inhibitor-1 mRNA, and protein in rat osteoblast-like cells (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 149 (1991), S. 34-43 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Transforming growth factor(β)(TGFβ) treatment of rat osteoblast-rich calvarial cells or of the clonal osteogenic sarcoma cells, UMR 106-01, resulted in dosedependent inhibition of plasminogen activator (PA) activity, and increased production of 3.2 kb mRNA and protein for PA inhibitor-1 (PAI-1). Although tissue-type PA(tPA) protein was not measured, TGF(β)did not influence production of mRNA for tPA. Production of 2.3 kb mRNA for urokinase-type PA (uPA) was also increased by TGF(β)in a dose-dependent manner. The effects of TGFβ on synthesis of mRNA for PAI-1 and uPA were maintained when protein synthesis was inhibited, and were abolished by inhibition of RNA synthesis. Although uPA had not been detected previously as a product of rat osteoblasts, treatment of lysates of osteoblast-like cells with plasmin yielded a band of PA activity on reverse fibrin autography, corresponding to a low Mr form of uPA. Untreated conditioned media from normal osteoblasts or UMR 106-01 cells contained no significant TGFβ activity, but activity could be detected in acidified medium. Treatment of conditioned media with plasmin resulted in activation of approximately 50% of the TGFβ detectable in acidified media. The results identify several effects of TGFβ on the PA-PA inhibitor system in osteoblasts. Net regulation of tPA activity through the stimulatory actions of several calciotropic hormones and the promotion of PAI-1 formation by TGFβ could determine the amount of osteoblast-derived TGFβ activated locally in bone. Stimulation of osteoblast production of mRNA for uPA could reflect effects on the synthesis of sc-uPA, a precursor for the active form of the enzyme.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041490106
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  • 7
    Electronic Resource
    Electronic Resource
    Ultrastructure of thyroid follicular cells following hypophysial portal vascular infusion of thyrotropin-releasing hormone (1978)
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 151 (1978), S. 145-151 
    Details
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Ultrastructural changes in thyroid follicular cell morphology were studied following the infusion of thyrotropin-releasing hormone (TRH) for 1 min into a hypophysial stalk portal vessel of adult male rats. At 1, 5, 15 and 30 min following infusion, thyroid glands were removed and prepared for electron microscopic examination. Thyroid follicular cells in unoperated, sham-operated non-infused, and saline-infused control rats were cuboidal, generally lacked intracellular colloid droplets and contained variable numbers of electron-dense lysosome-like bodies distributed throughout the cytoplasm. In experimental animals, marked intracellular colloid droplet accumulation was observed 5 min after TRH infusion and remained a constant finding throughout the time-periods studied. Numerous lysosome-like dense bodies accumulated in the apical cytoplasm of thyroid follicular cells at 30 min. Fusion of colloid droplets and lysosome-like bodies had apparently occurred by 30 min. At this time the colloid droplets were smaller, more electron-dense and were often located more basally within the follicular cell cytoplasm. This study suggests that the morphological response of thyroid follicular cells to hypophysial portal vascular infusion of TRH occurs rapidly and mimics, both temporally and morphologically, the response observed following systemic administration of exogenous TSH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001510113
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