Calcium in osteoblast-enriched bone cells

Imai, Kiyoshi; Neuman, M.W.; Kawase, Toshio; Saito, Shigeru

doi:10.1016/8756-3282(92)90200-g

Cited by 14 publications

(5 citation statements)

References 30 publications

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“…Whether the ion pair contributes to the endoplasmic reticulum, Ca 2þ response is at this time unknown. However, since osteoblasts accumulate considerable quantities of Ca 2þ [Imai et al, 1992], these cells would be particularly sensitive to modest fluxes in extracellular Pi levels. This observation may help to explain why osteoblast apoptosis is most marked at sites of rapid bone formation or resorption [Bronckers et al, 1996;Noble et al, 1997;Jilka et al, 1998Jilka et al, , 1999Weinstein et al, 1998].…”

Section: Discussionmentioning

confidence: 99%

Matrix regulation of skeletal cell apoptosis III: Mechanism of ion pair‐induced apoptosis

Saunders

Szymczyk

Shapiro

et al. 2006

J of Cellular Biochemistry

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Our previous work has demonstrated that while the Ca(2+) and Pi ions acting in concert function as a potent osteoblast apoptogen, the underlying mechanisms by which it activates cell death is not known. We hypothesize that the ion pair causes release of Ca(2+) from intracellular stores ([Ca(2+)]i); the increase in intracellular calcium prompts the mitochondria to uptake more calcium. This accumulation of calcium eventually results in the loss of mitochondrial membrane potential (MMP) and, subsequently, apoptosis. To test this hypothesis, we evaluated apoptosome formation in MC3T3-E1 osteoblast-like cells treated with the ion pair. Western blot analysis indicated migration of cytochrome-c and Smac/DIABLO from mitochondria to the cytoplasm. Inhibition of either the electron transfer chain (with antimycin a and rotenone), or the activation of a MMP transition (with bongkrekic acid) inhibited apoptosis in a dose-dependent manner. Pre-treating osteoblasts with ruthenium red, a Ca(2+) uniporter inhibitor of both mitochondria and the endoplasmic reticulum (ER), also completely abolished Ca(2+.)Pi-induced apoptosis. Moreover, we showed that an increase in [Ca(2+)]i preceded the increase in MMP over the first 45 min of treatment; a mitochondrial membrane permeability transition was evident at 75 min. To determine the role of ER, Ca(2+) stores in the generation of the apoptotic signal by the ion pair, cells were treated with several inhibitors. Apoptosis was inhibited when cells were treated with dantrolene, an inhibitor of ER ryanodine receptors, and 2-aminodiphenylborate, an IP3 Ca(2+) channel inhibitor, but not cyclopiazonic acid, an ER Ca(2)-ATPase inhibitor. Together, these data demonstrate that Ca(2+) Pi-induced osteoblast apoptosis is characterized by the generation of an apoptosome and that Ca(2+) release from ER stores may promote ion pair-dependent cell death.

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Section: Discussionmentioning

confidence: 99%

Matrix regulation of skeletal cell apoptosis III: Mechanism of ion pair‐induced apoptosis

Saunders

Szymczyk

Shapiro

et al. 2006

J of Cellular Biochemistry

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“…The closer that the osteoblast is to the mineralization site, the more Ca 2þ it will possess. 60 Therefore, the decrease of soluble Ca 2þ and PO 4 2À in the culture media can be also interpreted as a sign of progressive biomineralization due to immobilization of these ions within the hydroxapatite lattice. , and collagen I (c) in culture media at days 4, 14, and 28 in human bone marrow-derived cells, exposed to different stimuli.…”

Section: Dexamethasone Modulates Bmp-2 Effects On Mscmentioning

confidence: 99%

Dexamethasone modulates BMP‐2 effects on mesenchymal stem cells in vitro

Jäger

Fischer

Dohrn

et al. 2008

Journal Orthopaedic Research

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Dexamethasone/ascorbic acid/glycerolphosphate (DAG) and bone morphogenic protein (BMP)-2 are potent agents in cell proliferation and differentiation pathways. This study investigates the in vitro interactions between dexamethasone and BMP-2 for an osteoblastic differentiation of mesenchymal stem cells (MSCs). Bone marrow-derived human MSCs were cultured with DAG (group A), BMP-2 þ DAG (group B), and DAG þ BMP-2 combined with a porous collagen I/III scaffold (group C). RT-PCR, ELISA, immuncytochemical stainings and flow cytometry analysis served to evaluate the osteogenic-promoting potency of each of the above conditions in terms of cell morphology/viability, antigen presentation, and gene expression. DAG induced collagen I secretion from MSCs, which was further increased by the combination of DAG þ BMP-2. In comparison, the collagen scaffold and the control samples showed no significant influence on collagen I secretion of MSCs. DAG stimulation of MSCs led also to a steady but not significant increase of BMP-2 level. A DAG and more, a DAG þ BMP-2, stimulation increased the number of mesenchymal cells (CD105þ/CD73þ). All samples showed mRNA of ALP, osteopontin, Runx2, Twist 1 and 2, Notch-1/2, osteonectin, osteocalcin, BSP, and collagen-A1 after 28 days of in vitro culture. Culture media of all samples showed a decrease in Ca 2þ and PO 4 2À concentration, whereas a collagen-I-peak only occurred at day 28 in DAG-and DAG þ BMP-2-stimulated bone marrow cells. In conclusion, BMP-2 enhances DAG-induced osteogenic differentiation in mesenchymal bone marrow cells. Both agents interact in various ways and can modify osteoblastic bone formation. ß

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“…Moreover, abundant Ca 2+ and PO 4 3− can be used in ions mobilization and take part in the cell calcification, which plays another important role in biomineralization besides precipitation [25, 26]. Combined with the better cell calcification, the FHA-coated Mg alloys have the ability to have CDHA formation.…”

Section: Discussionmentioning

confidence: 99%

The Bioactivated Interfacial Behavior of the Fluoridated Hydroxyapatite-Coated Mg-Zn Alloy in Cell Culture Environments

Cao

Song

et al. 2011

Bioinorganic Chemistry and Applications

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A partially fluorine substituted hydroxyapatite- (FHA-) coated Mg-Zn alloy was prepared to investigate the interfacial behavior of degradable Mg-based biomaterials with degradable bioactive coatings in a cell culture environment. Peaks from the results of X-ray diffraction (XRD) were characterized and compared before and after cell culture. It was found that Ca-P, including poorly crystalline ion-substituted Ca-deficient HA (CDHA), was formed in greater amounts on the interface of coated samples compared with the uncoated ones. A thermodynamic mechanism for Ca-P formation on biodegradable Mg alloys in a cell culture environment is proposed. Combined with improved cell calcification, the-FHA coated Mg alloys have the ability to promote CDHA formation, as expected thermodynamically. It is suggested that the specific cell culture environment and the bone-like FHA coatings together facilitate the observed behavior. Moreover, cell culture environment probably increased the biomineralization to a detectable level by affecting the kinetics of apatite formation.

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Calcium in osteoblast-enriched bone cells

Cited by 14 publications

References 30 publications

Matrix regulation of skeletal cell apoptosis III: Mechanism of ion pair‐induced apoptosis

Matrix regulation of skeletal cell apoptosis III: Mechanism of ion pair‐induced apoptosis

Dexamethasone modulates BMP‐2 effects on mesenchymal stem cells in vitro

The Bioactivated Interfacial Behavior of the Fluoridated Hydroxyapatite-Coated Mg-Zn Alloy in Cell Culture Environments

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