2010Zhongguo yaolixue tongbaoRequires access

ERK 1/2 and p38 MAPK mediate the effect of BAPTA-AM inhibiting RANKL-induced bone marrow macrophages differentiation

XU Li-peng

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Abstract

Aim To explore whether ERK 1 /2 and p38 MAPK could mediate the effect of BAPTA-AM inhibiting RANKL-induced bone marrow macrophages differentiation.Methods BMMs were cultured with various concentrations of BAPTA-AM in the presence of MCSF(25 μg·L-1) and RANKL(25 μg·L-1) for 7 days,osteoclastogenic ability,osteoclast survival and the expression of phosphorylated ERK1 /2 and p38 MAPK were measured by TRAP staining and Western blot.Results BAPTA-AM inhibited osteoclastogenesis and osteoclast survival of BMMs by RANKL induction.The immunoblotting data revealed that BAPTA-AM could inhibit the phosphorylation of ERK1 /2 and p38 MAPK which were activated by RANKL.Conclusion ERK 1 /2 and p38 MAPK can mediate the effect of BAPTA-AM inhibiting osteoclastogenic ability of BMMs.This finding may be useful in the development of an osteoclastic inhibitor that targets intracellular signaling factors.

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Aim To explore whether ERK 1 /2 and p38 MAPK could mediate the effect of BAPTA-AM inhibiting RANKL-induced bone marrow macrophages differentiation.Methods BMMs were cultured with various concentrations of BAPTA-AM in the presence of MCSF(25 μg·L-1) and RANKL(25 μg·L-1) for 7 days,osteoclastogenic ability,osteoclast survival and the expression of phosphorylated ERK1 /2 and p38 MAPK were measured by TRAP staining and Western blot.Results BAPTA-AM inhibited osteoclastogenesis and osteoclast survival of BMMs by RANKL induction.The immunoblotting data revealed that BAPTA-AM could inhibit the phosphorylation of ERK1 /2 and p38 MAPK which were activated by RANKL.Conclusion ERK 1 /2 and p38 MAPK can mediate the effect of BAPTA-AM inhibiting osteoclastogenic ability of BMMs.This finding may be useful in the development of an osteoclastic inhibitor that targets intracellular signaling factors.

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Available abstract

Aim To explore whether ERK 1 /2 and p38 MAPK could mediate the effect of BAPTA-AM inhibiting RANKL-induced bone marrow macrophages differentiation.Methods BMMs were cultured with various concentrations of BAPTA-AM in the presence of MCSF(25 μg·L-1) and RANKL(25 μg·L-1) for 7 days,osteoclastogenic ability,osteoclast survival and the expression of phosphorylated ERK1 /2 and p38 MAPK were measured by TRAP staining and Western blot.Results BAPTA-AM inhibited osteoclastogenesis and osteoclast survival of BMMs by RANKL induction.The immunoblotting data revealed that BAPTA-AM could inhibit the phosphorylation of ERK1 /2 and p38 MAPK which were activated by RANKL.Conclusion ERK 1 /2 and p38 MAPK can mediate the effect of BAPTA-AM inhibiting osteoclastogenic ability of BMMs.This finding may be useful in the development of an osteoclastic inhibitor that targets intracellular signaling factors.

Key concepts: RANKL, Osteoclast, MAPK/ERK pathway, p38 mitogen-activated protein kinases, BAPTA, Chemistry, Cell biology, Bone marrow

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ERK 1/2 and p38 MAPK mediate the effect of BAPTA-AM inhibiting RANKL-induced bone marrow macrophages differentiation — Research Paper | ScholarLens