β Scribed by Shinrye Lee; Won-Ha Lee; Myung-Shik Lee; Kiyoshi Mori; Kyoungho Suk
No coin nor oath required. For personal study only.
A secreted protein, lipocalinβ2 (LCN2), has been previously shown to regulate a variety of cellular phenotypes such as cell death, migration, and morphology. The role of LCN2, however, appears to be different depending on the cellular context. Here, we investigated how LCN2 influences neuronal phenotypes by using primary cortical neuronal cell cultures and neuroblastoma cell lines as a model. When exposed to LCN2 protein, neurons and neuroblastoma cells were sensitized to cell death evoked by nitric oxide, oxidative stress, and tumor necrosis factorβΞ± (TNFβΞ±). A forced expression of lcn2 in glia enhanced neuronal cell death in cocultures of glia and neurons, indicating that both exogenous protein addition and endogenous expression of lcn2 give rise to similar results. Iron and BCL2βinteracting mediator of cell death (BIM) protein were involved in LCN2βinduced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)βmediated knockdown of bim expression. Furthermore, cell migration assay and immunofluorescence microscopic observation revealed that LCN2 accelerated neuronal motility and process extension, suggesting multiple roles for LCN2 in the regulation of neuronal cell death, migration, and morphology. Β© 2011 Wiley Periodicals, Inc.
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