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  • 1
    Electronic Resource
    Electronic Resource
    Differential Effect of High Extracellular Ca2+ on K+ and Cl− Conductances in Murine Osteoclasts (1997)
    Springer
    The journal of membrane biology 158 (1997), S. 59 -67 
    Details
    ISSN: 1432-1424
    Keywords: Key words: Osteoclast — Extracellular Ca2+— Cl− current — K+ current — G proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. Effects of the extracellular Ca2+ concentration ([Ca2+] o ) on whole cell membrane currents were examined in mouse osteoclastic cells generated from bone marrow/stromal cell coculture. The major resting conductance in the presence of 1 mm Ca2+ was mediated by a Ba2+-sensitive, inwardly rectifying K+ (IRK) current. A rise in [Ca2+] o (5–40 mm) inhibited the IRK current and activated an 4,4′-diisothiocyano-2,2′-stilbenedisulfonate (DIDS)-sensitive, outwardly rectifying Cl− (ORCl) current. The activation of the ORCl current developed slowly and needed higher [Ca2+] o than that required to inhibit the IRK current. The inhibition of the IRK current consisted of two components, initial and subsequent late phases. The initial inhibition was not affected by intracellular application of guanosine 5′-O-(3-thiotriphosphate) (GTPγS) or guanosine 5′-O-(2-thiodiphosphate) (GDPβS). The late inhibition, however, was enhanced by GTPγS and attenuated by GDPβS, suggesting that GTP-binding proteins mediate this inhibition. The activation of the ORCl current was suppressed by pretreatment with pertussis toxin, but not potentiated by GTPγS. An increase in intracellular Ca2+ level neither reduced the IRK current nor activated the ORCl current. Staurosporine, an inhibitor for protein kinase C, did not modulate the [Ca2+] o -induced changes in the IRK and ORCl conductances. These results suggest that high [Ca2+] o had a dual action on the membrane conductance of osteoclasts, an inhibition of an IRK conductance and an activation of an ORCl conductance. The two conductances modulated by [Ca2+] o may be involved in different phases of bone resorption because they differed in Ca2+ sensitivity, temporal patterns of changes and regulatory mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002329900243
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanism of atherosclerotic calcification (2000)
    Springer
    Zeitschrift für Kardiologie 89 (2000), S. S075 
    Details
    ISSN: 1435-1285
    Keywords: Key words Alkaline phosphatase – atherosclerosis – calciotropic hormones – 1α-hygroxylase – macrophages – osteoblastic differentiation – sodium-dependent phosphate cotransport – vascular smooth muscle cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Calcification is almost invariably associated with atherosclerotic plaque lesions. Recent data suggest that plaque calcification is an active, regulated process similar to osteogenesis. In order to clarify the mechanism of plaque calcification, we developed an in vitro model of vascular calcification by utilizing bovine vascular smooth muscle cells (BVSMCs). This model is useful in that diffuse and massive calcification can be induced within 2 weeks and thereby biochemical analyses of vascular calcification can be performed. We have analyzed several aspects of vascular calcification by using this model and demonstrated as follows: 1) in vitro calcification of BVSMCs is regulated by calciotropic hormones and BVSMCs are equipped with a unique autocrine and/or paracrine system regulating calcium metabolism. 2) Sodium-dependent phosphate cotransport plays a crucial role in BVSMC calcification as well as in mineralization of skeletal tissues. 3) BVSMCs acquire osteoblastic phenotype under certain conditions. Finally, we discuss the roles of macrophages in the development of atherosclerotic calcification. Interferon-γ (INF-γ) induces gene expression of 25-hydrovitamin D-1α-hydroxylase (1αOhase) and its activity in macrophages. Since 1αOhase can locally convert 25-hydroxyvitamin D into 1α,25-dihydroxyvitamin D (1,25(OH)2D), an active metabolite of vitamin D, it is suggested that local production of 1,25(OH)2D by macrophages may promote atherosclerotic calcification. Moreover, macrophages may be involved in the phenotypic changes of vascular smooth muscle cells (VSMCs) to acquire calcifying capacity. Therefore, the phenotypic changes of VSMCs in atherosclerotic plaque may contribute to the development of atherosclerotic calcification.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003920070103
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  • 3
    Electronic Resource
    Electronic Resource
    Enrichment of generated murine osteoclasts (1994)
    Springer
    Calcified tissue international 55 (1994), S. 387-394 
    Details
    ISSN: 1432-0827
    Keywords: Osteoclasts ; ST-2 cells ; CSF-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract Biochemical and molecular studies of osteoclasts generally require cells in a reasonable degree of purity. The chicken has been extremely useful in this regard, as abundant avian osteoclasts can be generated in vitro entirely from pure populations of marrow macrophage precursors. Propagation of murine osteoclasts is, in contrast, far less efficients, demanding the presence of stromal cells. The aims of this study were to develop a method by which murine osteoclasts generated in culture, can be effectively enriched while maintaining viability and, to explore the mechanisms by which stromal cells promote murine osteoclast generation and survival. We find that 106 fractionated murine marrow cells enriched, for marrow-residing colony-forming units (CFU-cs), yield 3000–4000 tartrate-resistant acid phosphatase (TRAP)-expressing multinucleated giant cells when cultured for 12 days with ST-2 stromal cells. These cells are osteoclasts as evidenced by their ability to “pit” bone slices, resorb radiolabeled bone particles, and generate cyclic AMP in response to calcitonin. Treatment of these generated osteoclast cultures with bacterial collagenase for 2 hours at 37° selectively removes virtually all ST-2 cells, yielding a 〉60% pure population of TRAP and calcitonin receptor-expressing cells, 90% of which are viable. These cells continue to respond to calcitonin and survive for 24 hours in the absence of ST-2 cells. We also found that murine osteoclast generation depends upon contact of osteoclast precursors with viable ST-2 cells. Furthermore, the stromal cells secrete macrophage colony-stimulating factor (CSF-1), and the anti-CSF-1 antibody 5A1 inhibits murine osteoclastogenesis. Exogenous CSF-1, in turn, partially overrides the anti-osteoclastogenic effect of 5A1. We conclude that (1) the purity of murine osteoclasts generated from bone marrow cells enriched for CFU-cs can be greatly enhanced by selective removal of associated stromal cells, and (2) both soluble and membraneresiding stromal cell factors are necessary for generation of murine osteoclasts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00299320
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  • 4
    Electronic Resource
    Electronic Resource
    Poor Glycemic Control Impairs the Response of Biochemical Parameters of Bone Formation and Resorption to Exogenous 1,25-Dihydroxyvitamin D3 in Patients with Type 2 Diabetes (1999)
    Springer
    Osteoporosis international 9 (1999), S. 525-531 
    Details
    ISSN: 1433-2965
    Keywords: Key words:1,25(OH)2D – Diabetes mellitus – Diabetic osteopenia – Osteocalcin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Osteoblast deficit plays a principal role in the development of diabetic osteopenia. We have previously reported that high glucose conditions impair the function of osteoblast-like MG-63 cells. This study was performed to assess the sensitivity of osteoblasts to 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in patients with type 2 diabetes without insulin deficiency or overt diabetic complications. During stimulation with 1,25(OH)2D3 at 2.0 mg/day for 6 consecutive days in 9 type 2 diabetic patients, serum levels of bone alkaline phosphatase (BALP), osteocalcin (OC) and the carboxyterminal propeptide of type 1 procollagen, and the urinary excretion of pyridinoline and deoxypyridinoline (DPYR), were monitored. As parameters of glycemic control, the mean level of fasting plasma glucose (mFPG) throughout the 1,25(OH)2D3 stimulation test and the level of HbA1C were used. 1,25(OH)2D3 increased serum 1,25(OH)2D significantly by day 2, which was followed by a significant reduction in the serum level of intact parathyroid hormone. The maximal increment of serum OC adjusted for that of 1,25(OH)2D was negatively correlated with both mFPG and HbA1C levels (p50.05). Furthermore, the magnitude of 1,25(OH)2D3-induced bone resorption, as reflected by the maximal increase in urinary DPYR excretion, was negatively correlated with the mFPG level (p50.05). Basal BALP tended to be negatively correlated with HbA1C, although not to a significant extent. In conclusion, our findings would indicate that poor glycemic control impairs the responses of osteoblasts and osteoclasts to 1,25(OH)2D3 in normo-insulinemic type 2 diabetic patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001980050180
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