rankl increases the level of mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitrorankl的mcl1水平增加破骨细胞,减少bisphosphonate-induced体外破骨细胞凋亡.pdfVIP

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rankl increases the level of mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitrorankl的mcl1水平增加破骨细胞,减少bisphosphonate-induced体外破骨细胞凋亡.pdf

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rankl increases the level of mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitrorankl的mcl1水平增加破骨细胞,减少bisphosphonate-induced体外破骨细胞凋亡

Available online /content/11/2/R58 Vol 11 No 2 Open Access Research article RANKL increases the level of Mcl-1 in osteoclasts and reduces bisphosphonate-induced osteoclast apoptosis in vitro Karen A Sutherland*, Helena L Rogers*, Denise Tosh and Michael J Rogers Bone Musculoskeletal Research Programme, School of Medicine Dentistry, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK * Contributed equally Corresponding author: Michael J Rogers, m.j.rogers@abdn.ac.uk Received: 25 Jun 2008 Revisions requested: 31 Jul 2008 Revisions received: 8 Apr 2009 Accepted: 30 Apr 2009 Published: 30 Apr 2009 Arthritis Research Therapy 2009, 11:R58 (doi:10.1186/ar2681) This article is online at: /content/11/2/R58 © 2009 Sutherland et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction Bisphosphonates are the most widely used class Results RANKL significantly attenuated the ability of both of drug for inhibiting osteoclast-mediated bone loss, but their clodronate and alendronate to induce osteoclast apoptosis and effectiveness at preventing joint destruction in rheumatoid inhibit bone resorption. Treatment of rabbit osteoclasts with arthritis has generally been disappointing. We examined RANKL was associated with an increase in the anti-apoptotic whether the ability of bisphosphonates to induce osteoclast protein Mcl-1