Gap-junctional communication mediates parathyroid hormone stimulation of mineralization in osteoblastic cultures

Previously we showed that physiological levels of parathyroid hormone (PTH) can increase the mineralization of extracellular matrix (ECM) by osteoblast-like cells in vitro. In this study, we assess the role of gap-junctional intercellular communication (GJC) in the PTH-enhanced mineralization of ECM...

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Bibliographic Details
Published in:Bone (New York, N.Y.) N.Y.), 2001, Vol.28 (1), p.38-44
Main Authors: Schiller, P.C, D’Ippolito, G, Balkan, W, Roos, B.A, Howard, G.A
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Biomineralization
Calcification, Physiologic - drug effects
Cell Communication - drug effects
Cell Communication - physiology
Cell coupling
Cell Differentiation - physiology
Cells, Cultured
Connexin 43 - metabolism
Connexin-43 (Cx43)
Fundamental and applied biological sciences. Psychology
Gap junctions
Gap Junctions - physiology
Mice
Osteoblasts
Osteoblasts - cytology
Osteoblasts - drug effects
Osteoblasts - metabolism
Parathyroid hormone (PTH)
Parathyroid Hormone - pharmacology
Skeleton and joints
Vertebrates: osteoarticular system, musculoskeletal system
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Summary:Previously we showed that physiological levels of parathyroid hormone (PTH) can increase the mineralization of extracellular matrix (ECM) by osteoblast-like cells in vitro. In this study, we assess the role of gap-junctional intercellular communication (GJC) in the PTH-enhanced mineralization of ECM in MC3T3-E1 cells, a murine culture model of osteoblastic differentiation. Messenger RNA and protein for connexin 43 (Cx43), the major component of MC3T3-E1 gap junctions, and GJC increased as the cells progressed toward a mature phenotype. Immunocytochemistry showed accumulation of Cx43 at the area of close contact between cells. The timing of the PTH treatment that increased matrix mineralization in these cells coincided with the highest expression of Cx43 and GJC. Administration of 18-α-glycyrrhetinic acid (AGA) promptly blocked GJC in cultures of MC3T3-E1 cells in a dose-dependent and reversible manner at all times tested during the culture period. Treatment with AGA, but not with an inactive analog, reversed the PTH-induced ECM mineralization. These data suggest that GJC mediates anabolic actions of PTH related to osteoblast-mediated mineralization.
ISSN:8756-3282
1873-2763
DOI:10.1016/S8756-3282(00)00412-9