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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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Background: Lipocalin-2 (LCN2), a small glycoprotein, has a pivotal role in diverse biological processes such as cellular proliferation and differentiation. We previously reported that LCN2 is implicated in osteoclast formation induced by receptor activator of nuclear factor-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF).
In the present study, we used a knockout mouse model to further investigate the role of LCN2 in osteoclast development. Methods: Osteoclastogenesis was assessed using primary bone marrow-derived macrophages. RANKL and M-CSF signaling was determined by immunoblotting, cell proliferation by bromodeoxyuridine (BrdU) enzyme-linked immunosorbent assay (ELISA), and apoptosis by cell death detection ELISA. Bone morphometric parameters were determined using a micro-computed tomography system. Results: Our results showed that LCN2 deficiency increases tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclast formation in vitro, a finding that reflects enhanced proliferation and differentiation of osteoclast lineage cells. LCN2 deficiency promotes M-CSF-induced proliferation of bone marrow macrophages (BMMs), osteoclast precursors, without altering their survival. The accelerated proliferation of LCN2-deficient precursors is associated with enhanced expression and activation of the M-CSF receptor, c-Fms. Furthermore, LCN2 deficiency stimulates the induction of c-Fos and nuclear factor of activated T cells c1 (NFATc1), key transcription factors for osteoclastogenesis, and promotes RANKL-induced inhibitor of kappa B (IκBα) phosphorylation. Interestingly, LCN2 deficiency does not affect basal osteoclast formation in vivo, suggesting that LCN2 might play a role in the enhanced osteoclast development that occurs under some pathological conditions. Conclusions: Our study establishes LCN2 as a negative modulator of osteoclast formation, results that are in accordance with our previous findings.
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참고문헌 (31)
참고문헌 신청
Boyle WJ / 2003 / Osteoclast differentiation and activation / Nature 423:337~342
Teitelbaum SL / 2003 / Genetic regulation of osteoclast development and function / Nat Rev Genet 4:638~649
Jaworowski A / 1999 / Roles of the mitogen-activated protein kinase family in macrophage responses to colony stimulating factor-1 addition and withdrawal / J Biol Chem 274:15127~15133
Takeshita S / 2007 / c-Fms tyrosine 559 is a major mediator of M-CSF-induced proliferation of primary macrophages / J Biol Chem 282:18980~18990
Valledor AF / 2000 / The differential time-course of extracellular-regulated kinase activity correlates with the macrophage response toward proliferation or activation / J Biol Chem 275:7403~7409
Teitelbaum SL / 2003 / Genetic regulation of osteoclast development and function / Nat Rev Genet 4:638~649
Jaworowski A / 1999 / Roles of the mitogen-activated protein kinase family in macrophage responses to colony stimulating factor-1 addition and withdrawal / J Biol Chem 274:15127~15133
Takeshita S / 2007 / c-Fms tyrosine 559 is a major mediator of M-CSF-induced proliferation of primary macrophages / J Biol Chem 282:18980~18990
Valledor AF / 2000 / The differential time-course of extracellular-regulated kinase activity correlates with the macrophage response toward proliferation or activation / J Biol Chem 275:7403~7409
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