| First Author | Mesquita SD | Year | 2014 |
| Journal | Cell Death Differ | Volume | 21 |
| Issue | 10 | Pages | 1588-99 |
| PubMed ID | 24853299 | Mgi Jnum | J:230013 |
| Mgi Id | MGI:5755220 | Doi | 10.1038/cdd.2014.68 |
| Citation | Mesquita SD, et al. (2014) Lipocalin 2 modulates the cellular response to amyloid beta. Cell Death Differ 21(10):1588-99 |
| abstractText | The production, accumulation and aggregation of amyloid beta (Abeta) peptides in Alzheimer's disease (AD) are influenced by different modulators. Among these are iron and iron-related proteins, given their ability to modulate the expression of the amyloid precursor protein and to drive Abeta aggregation. Herein, we describe that lipocalin 2 (LCN2), a mammalian acute-phase protein involved in iron homeostasis, is highly produced in response to Abeta1-42 by choroid plexus epithelial cells and astrocytes, but not by microglia or neurons. Although Abeta1-42 stimulation decreases the dehydrogenase activity and survival of wild-type astrocytes, astrocytes lacking the expression of Lcn2 are not affected. This protection results from a lower expression of the proapoptotic gene Bim and a decreased inflammatory response. Altogether, these findings show that Abeta toxicity to astrocytes requires LCN2, which represents a novel mechanism to target when addressing AD. |
