{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,27]],"date-time":"2025-06-27T04:04:40Z","timestamp":1750997080022},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,10,28]],"date-time":"2009-10-28T00:00:00Z","timestamp":1256688000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2010,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We have analyzed the effect of the synthetic glucocorticoid dexamethasone, used alone or in combination with recombinant TRAIL, on in vitro osteoclastic differentiation of peripheral blood\u2010derived macrophages cultured in the presence of macrophage\u2010colony stimulating factor (M\u2010CSF)\u2009+\u2009RANKL for 12\u201314 days. Dexamethasone exhibited different effects based on the concentration used. Indeed, while at 10<jats:sup>\u22127<\/jats:sup>\u2009M dexamethasone reduced the number of mature osteoclasts, at 10<jats:sup>\u22128<\/jats:sup>\u2009M showed no significant effects and at 10<jats:sup>\u22129<\/jats:sup>\u2009M significantly increased the number of mature osteoclasts, with respect to cells cultured with only M\u2010CSF\u2009+\u2009RANKL. On the other hand, the addition in culture of recombinant TRAIL inhibited the output of mature osteoclasts induced by M\u2010CSF\u2009+\u2009RANKL. However, the presence of dexamethasone (10<jats:sup>\u22128<\/jats:sup> or 10<jats:sup>\u22129<\/jats:sup>\u2009M) into the culture medium significantly counteracted the anti\u2010osteoclastic activity of TRAIL. In order to ascertain whether dexamethasone, might also interfere with the anti\u2010leukemic activity of TRAIL, the degree of apoptosis induced by TRAIL was evaluated in several myeloid (OCI, MOLM, HL\u201060) and lymphoid (SKW6.4, MAVER, BJAB) leukemic cell lines. The levels of TRAIL\u2010triggered apoptosis were not significantly different between leukemic cells cultured in the absence or presence of dexamethasone. Concerning the molecular mechanism mediating the dexamethasone\u2010suppression of the TRAIL activity in pre\u2010osteoclasts, but not in leukemic cells, we found that dexamethasone induced a significant down\u2010regulation of the surface levels of TRAIL\u2010R2 in cells of the osteoclastic lineage but not in leukemic cells. The ability of dexamethasone to counteract the TRAIL pathway envisions a novel mechanism mediating the pro\u2010osteoclastic activity of dexamethasone in vivo. J. Cell. Physiol. 222: 357\u2013364, 2010. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21960","type":"journal-article","created":{"date-parts":[[2009,10,29]],"date-time":"2009-10-29T20:03:19Z","timestamp":1256846599000},"page":"357-364","source":"Crossref","is-referenced-by-count":10,"title":["Dexamethasone counteracts the anti\u2010osteoclastic, but not the anti\u2010leukemic, activity of TNF\u2010related apoptosis inducing ligand 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