High Extracellular Calcium Increased Expression of Ank, PC-1 andOsteopontin in Mouse Calvarial Cells
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In the process of bone remodeling, mineral phase of bone is dissolved by osteoclasts, resulting in elevation of calcium concentration in micro-environment. This study was performed to explore the effect of high extracellular calcium (Ca ²+ e) on mineralized nodule formation and on the expression of progressive ankylosis (Ank), plasma cell membrane glycoprotein-1 (PC-1) and osteopontin by primary cultured mouse calvarial cells. Osteoblastic differentiation and mineralized nodule formation was induced by culture of mouse calvarial cells in osteoblast differentiation medium containing ascorbic acid and β-glycerophosphate. Although Ank, PC-1 and osteopontin are well known inhibitors of mineralization, expression of these genes were induced at the later stage of osteoblast differentiation during when expression of osteocalcin, a late marker gene of osteoblast differentiation, was induced and mineralization was actively progressing. High Ca ²+ e (10 mM) treatment highly enhanced mRNA expression of Ank, PC-1 and osteopontin in the late stage of osteoblast differentiation but not in the early stage. Inhibition of p44/42 MAPK activation but not that of protein kinase C suppressed high Ca ²+ e-induced expression of Ank, PC-1 and osteopontin. When high Ca ²+ e (5 mM or 10 mM) was present in culture medium during when mineral deposition was actively progressing, matrix calcifiation was significantly increased by high Ca ²+ e. This stimulatory effect was abolished by pyrophosphate (5 mM) or levamisole (0.1-0.5 mM), an alkaline phosphatase inhibitor. In addition, probenecid (2mM), an inhibitor of Ank, suppressed matrix calcification in both control and high Ca ²+ e-treated group, suggesting the possible role of Ank in matrix calcification by osteoblasts. Taken together, these results showed that high Ca ²+ e stimulates expression of Ank, PC-1 and osteopontin as well as matrix calcification in late differentiation stage of osteoblasts and that p44/42 MAPK activation is involved in high Ca ²+ e- induced expression of Ank, PC-1 and osteopontin.
Abstract
In the process of bone remodeling, mineral phase of bone is dissolved by osteoclasts, resulting in elevation of calcium concentration in micro-environment. This study was performed to explore the effect of high extracellular calcium (Ca ²+ e) on mineralized nodule formation and on the expression of progressive ankylosis (Ank), plasma cell membrane glycoprotein-1 (PC-1) and osteopontin by primary cultured mouse calvarial cells. Osteoblastic differentiation and mineralized nodule formation was induced by culture of mouse calvarial cells in osteoblast differentiation medium containing ascorbic acid and β-glycerophosphate. Although Ank, PC-1 and osteopontin are well known inhibitors of mineralization, expression of these genes were induced at the later stage of osteoblast differentiation during when expression of osteocalcin, a late marker gene of osteoblast differentiation, was induced and mineralization was actively progressing. High Ca ²+ e (10 mM) treatment highly enhanced mRNA expression of Ank, PC-1 and osteopontin in the late stage of osteoblast differentiation but not in the early stage. Inhibition of p44/42 MAPK activation but not that of protein kinase C suppressed high Ca ²+ e-induced expression of Ank, PC-1 and osteopontin. When high Ca ²+ e (5 mM or 10 mM) was present in culture medium during when mineral deposition was actively progressing, matrix calcifiation was significantly increased by high Ca ²+ e. This stimulatory effect was abolished by pyrophosphate (5 mM) or levamisole (0.1-0.5 mM), an alkaline phosphatase inhibitor. In addition, probenecid (2mM), an inhibitor of Ank, suppressed matrix calcification in both control and high Ca ²+ e-treated group, suggesting the possible role of Ank in matrix calcification by osteoblasts. Taken together, these results showed that high Ca ²+ e stimulates expression of Ank, PC-1 and osteopontin as well as matrix calcification in late differentiation stage of osteoblasts and that p44/42 MAPK activation is involved in high Ca ²+ e- induced expression of Ank, PC-1 and osteopontin.
참고문헌 (47)
- Adams, C.S., "Matrix regulation of skeletal cell apoptosis. Role of calcium and phosphate ions", Journal of Biological Chemistry, 276, pp.20316~20322 (2001)
- Addison, W.N., "Pyrophosphate inhibits mineralization of osteoblast cultures by binding to mineral, up-regulating osteopontin, and inhibiting alkaline phosphatase activity", Journal of Biological Chemistry, 282, pp.15872~15883 (2007)
- Anderson, H.C., "Impaired calcification around matrix vesicles of growth plate and bone in alkaline phosphatase-deficient mice", American Journal of Pathology, 164, pp.841~847 (2004)
- Anderson, H.C., "Sustained osteomalacia of long bones despite major improvement in other hypophosphatasia-related mineral deficits in tissue nonspecific alkaline phosphatase", nucleotide pyrophosphatase phosphodiesterase 1 double-deficient mice, 2005, pp.166, 1711~1720
- Aubin, J.E, "The osteoblast lineage. In Principles of Bone Biology", pp.51~67 (1996), Academic Press
- Beck, G.R. Jr., "Inorganic phosphate as a signaling molecule in osteoblast differentiation", Journal of Cellular Biochemistry, 90, pp.234~243 (2003)
- Beck, G.R. Jr., "Inorganic phosphate regulates multiple genes during osteoblast differentiation, including Nrf2", Experimental Cell Research, 288, pp.288~300 (2003)
- Bellows, C.G., "Initiation and progression of mineralization of bone nodules formed in vitro:the role of alkaline phosphatase and organic phosphate", Bone and Mineral, 14, pp.27~40 (1991)
- Bellows, C.G., "Inorganic phosphate added exogenously or released from beta-glycerophosphate initiates mineralization of osteoid nodules in vitro", Bone and Mineral, 17, pp.15~29 (1992)
- Brown, E.M., "Extracellular calcium sensing and extracellular calcium signaling", Physiological Reviews, 81, pp.239~297 (2001)
- Dvorak, M.M., "Ca 2+ as an extracellular signal in bone", Cell Calcium, 35, pp.249~255 (2004)
- 42 Mina Song, "Physiological changes in extracellular calcium concentration directly control osteoblast function in the absence of calciotropic hormones", Proceedings of the National Academy of Sciences of the United States of America, 통권 : 101, pp.5140~5145 (2004)
- Fedde, K.N., "Alkaline phosphatase knock-out mice recapitulate the metabolic and skeletal defects of infantile hypophosphatasia", Journal of Bone and Mineral Research, 14, pp.2015~2026 (1999)
- Godwin, S.L, "Extracellular calcium and platelet derived growth factor promote receptor-mediated chemotaxis in osteoblasts through different signaling pathways", Journal of Biological Chemistry, 272, pp.11307~11312 (1997)
- Hakim, F.T., "Hereditary joint disorder in progressive ankylosis (ank", ank) mice. I. Association of calcium hydroxyapatite deposition with inflammatory arthropathy, 1984, pp.27, 1411~1420
- Harmey, D., "Concerted regulation of inorganic pyrophosphate and osteopontin by akp2, enpp1,and ank: an integrated model of the pathogenesis of mineralization disorders", American Journal of Pathology, 164, pp.1199~1209 (2004)
- Harmey, D., "Elevated skeletal osteopontin levels contribute to the hypophosphatasia phenotype in Akp2(-", -) mice, 2006, pp.21, 1377~1386
- Hashimoto, S., "Chondrocyte-derived apoptotic bodies and calcification of articular cartilage. Proc", Proceedings of the National Academy of Sciences, 통권 : 95, pp.3094~3099 (1998)
- Hatch, N.E., "FGF2 alters expression of the pyrophosphate", phosphate regulating proteins, PC-1, ANK and TNAP, in the calvarial osteoblastic cell line, MC3T3E1(C4), 2005, pp.46, 184~192
- Hessle, L., "Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralization", Proceedings of the National Academy of Sciences of the United States of America, 통권 : 99, pp.9445~9949 (2002)
- Ho, A.M., "Role of mouse ank gene in control of tissue calcification and arthritis", Science, 289, pp.265~269 (2000)
- Hunter, G.K., "Modulation of crystal formation by bone phosphoproteins; structural specificity of the osteopontin-mediated inhibition of hydroxyapatite formation", Biochemical Journal, 300, pp.723~728 (1994)
- Johnson, K., "Upregulated ank expression in osteoarthritis can promote both chondrocyte MMP-13 expression and calcification via chondrocyte extracellular PPi excess", Osteoarthritis and Cartilage, 12, pp.321~335 (2004)
- Johnson, K., "Differential mechanisms of inorganic pyrophosphate production by plasma cell membrane glycoprotein-1 and B10 in chondrocytes", Arthritis and Rheumatism, 42, pp.1986~1997 (1999)
- Johnson, K., "Matrix vesicle plasma membrane glycoprotein-1 regulates mineralization by murine osteoblastic MC3T3 cells", Journal of Bone and Mineral Research, 14, pp.883~892 (1999)
- Johnson, K.A., "Osteoblast tissue-nonspecific alkaline phosphatase antagonizes and regulates PC-1", American Journal of Physiology - Regulatory Integrative and Comparative Physiology, 279, pp.R1365~R1377 (2000)
- Johnson, K., "Linked deficiencies in extracellular PP(i) and osteopontin mediate pathologic calcification associated with defective PC-1 and ANK expression", Journal of Bone and Mineral Research, 18, pp.994~1004 (2003)
- Jono, S., "Phosphorylation of osteopontin is required for inhibition of vascular smooth muscle cell calcification", Journal of Biological Chemistry, 275, pp.20197~20203 (2000)
- Jun, J.H., "N-acetylcysteine stimulates osteoblastic differentiation of mouse calvarial cells. J. Cell. Biochem", Journal of Cellular Biochemistry, 103, pp.1246~1255 (2008)
- 김형근, "Identification of Genes Modulated by High Extracellular Calcium in Coculture of Mouse Osteoblasts and Bone Marrow Cells by Oligo Chip Assay", International Journal of Oral Biology, 31(2), pp.53~65 (2006), 대한구강생물학회
- Kim, Y.H., "p44", 42 MAPK activation is necessary for receptor activator of nuclear factor-κB ligand induction by high extracellular calcium, 2003, pp.304, 729~735
- Lynch, M.P., "Apoptosis during bone-like tissue development in vitro", Journal of Cellular Biochemistry, 68, pp.31~49 (1998)
- Murshed, M., "Unique coexpression in osteoblasts of broadly expressed genes accounts for the spatial restriction of ECM mineralization to bone", Genes & Development, 19, pp.1093~1104 (2005)
- Nielsen, L.B., "Expression of type III sodium-dependent phosphate transporters", retroviral receptors mRNAs during osteoblast differentiation, 2001, pp.28, 160~166
- Okawa, A., "Mutation in Npps in a mouse model of ossification of the posterior longitudinal ligament of the spine", Nat. Genet, 19, pp.271~273 (1998)
- Proudfoot, D., "Apoptosis regulates human vascular calcification in vitro: evidence for initiation of vascular calcification by apoptotic bodies", Circulation Research, 87, pp.1055~1062 (2000)
- Rutsch, F., "PC-1 Nucleoside Triphosphate Pyrophosphohydrolase Deficiency in Idiopathic Infantile Arterial Calcification", American Journal of Pathology, 158, pp.543~554 (2001)
- Rutsch, F., "Mutations in ENPP1 are associated with 'idiopathic' infantile arterial calcification", Nature Genetics, 34, pp.379~381 (2003)
- Silver, I.A., "Microelectrode studies on the acid microenvironment beneath adherent macrophages and osteoclasts", Experimental Cell Research, 175, pp.266~276 (1988)
- Stein, G.S., "Mechanisms regulating osteoblast proliferation and differentiation. In Principles of Bone Biology. 1st ed.", pp.69~86 (1996), Academic Press
- Suzuki, A., "Enhanced expression of the inorganic phosphate transporter Pit-1 is involved in BMP-2-induced matrix mineralization in osteoblast-like cells", Journal of Bone and Mineral Research, 21, pp.674~683 (2006)
- Terkeltaub, R.A, "Cell Physiol", American Journal of Physiology - Cell Physiology, 281, pp.C1~C11 (2001)
- Wang, W., "Role of the progressive ankylosis gene (ank) in cartilage mineralization", Molecular and Cellular Biology, 25, pp.312~323 (2005)
- Whyte, M.P., "Hypophosphatasia and the role of alkaline phosphatase in skeletal mineralization", Endocrine Reviews, 15, pp.439~461 (1994)
- Yamaguchi, T., "Activation of p42", 44 and p38 mitogenactivated protein kinases by extracellular calcium-sensing receptor agonists induces mitogenic responses in the mouse osteoblastic MC3T3-E1 cell line, 2000, pp.279, 363~368
- Yamauchi, M., "Involvement of calcium-sensing receptor in osteoblastic differentiation of mouse MC3T3-E1 cells", American Journal of Physiology - Endocrinology and Metabolism, 288, pp.E608~E616 (2005)
- Zhu, J.X., "Temporal and spatial gene expression of major bone extracellular matrix molecules during embryonic mandibular osteogenesis in rats", Histochemical Journal, 33, pp.25~35 (2001)