Prostaglandin E 2 causes a transient inhibition of mineral mobilization, matrix degradation, and lysosomal enzyme release from mouse calvarial bones In Vitro

摘要: The effect of prostaglandin E2 (PGE2) on the kinetic bone resorptionin vitro was assessed by following release minerals and degradation matrix in cultured mouse calvarial bones. PGE2 (1 3 μmol/liter) caused an initial inhibition of45Ca, stable calcium, inorganic phosphate from unstimulated transient after 24 48 hours PGE2-treated bones enhanced. 0.3 μmol/liter stimulated of45Ca hours, but at this concentration no observed. inhibitory could be further increased three structurally different inhibitors cyclic AMP breakdown. not only mineral also degradation, as of3H [3H]-proline labeled In addition, (3 μmol/liter), presence phosphodiesterase inhibitor isobutylmethylxanthine, a rapid (6 hours) lysosomal enzymes β-glucuronidase β-N-acetyl-glucosaminidase, without affecting cytosolic enzyme lactate dehydrogenase. Similar specific seen calcitonin dibutyryl AMP, parathyroid hormone (PTH). Neither nor rolipram Ro 20.1724, inhibit stages PTH-induced45Ca release. Nor did stimulation radioactive calcium mobilization induced 1α(OH)-vitamin D3. Enhancement formation forskolin, choleratoxin, resulted reduction followed delayed (96 hours). These data indicate that has capacity to reduce activity unstimulated, preexisting osteoclasts AMP-dependent process.