دورية أكاديمية

Lipocalin 2 modulates the cellular response to amyloid beta.

التفاصيل البيبلوغرافية
العنوان: Lipocalin 2 modulates the cellular response to amyloid beta.
المؤلفون: Mesquita SD; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Ferreira AC; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Falcao AM; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Sousa JC; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Oliveira TG; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Correia-Neves M; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Sousa N; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Marques F; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal., Palha JA; 1] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal [2] ICVS/3B's-PT Government Associate Laboratory, Guimaraes, Portugal.
المصدر: Cell death and differentiation [Cell Death Differ] 2014 Oct; Vol. 21 (10), pp. 1588-99. Date of Electronic Publication: 2014 May 23.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 9437445 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5403 (Electronic) Linking ISSN: 13509047 NLM ISO Abbreviation: Cell Death Differ Subsets: MEDLINE
أسماء مطبوعة: Publication: <2003->: London : Nature Publishing Group
Original Publication: London : Edward Arnold, c1994-
مواضيع طبية MeSH: Acute-Phase Proteins/*genetics , Amyloid beta-Peptides/*pharmacology , Apoptosis Regulatory Proteins/*biosynthesis , Astrocytes/*metabolism , Lipocalins/*biosynthesis , Lipocalins/*genetics , Membrane Proteins/*biosynthesis , Oncogene Proteins/*genetics , Proto-Oncogene Proteins/*biosynthesis, Alzheimer Disease ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Astrocytes/cytology ; Bcl-2-Like Protein 11 ; Cells, Cultured ; Epithelial Cells/metabolism ; Heme Oxygenase (Decyclizing)/biosynthesis ; Inflammation/immunology ; Iron/metabolism ; Lipocalin-2 ; Mice ; Mice, Inbred C57BL ; Microglia/metabolism ; Neurons/metabolism ; Rats
مستخلص: The production, accumulation and aggregation of amyloid beta (Aβ) 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 Aβ aggregation. Herein, we describe that lipocalin 2 (LCN2), a mammalian acute-phase protein involved in iron homeostasis, is highly produced in response to Aβ1-42 by choroid plexus epithelial cells and astrocytes, but not by microglia or neurons. Although Aβ1-42 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 Aβ toxicity to astrocytes requires LCN2, which represents a novel mechanism to target when addressing AD.
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المشرفين على المادة: 0 (Acute-Phase Proteins)
0 (Amyloid beta-Peptides)
0 (Amyloid beta-Protein Precursor)
0 (Apoptosis Regulatory Proteins)
0 (Bcl-2-Like Protein 11)
0 (Bcl2l11 protein, mouse)
0 (Bcl2l11 protein, rat)
0 (Lcn2 protein, rat)
0 (Lipocalin-2)
0 (Lipocalins)
0 (Membrane Proteins)
0 (Oncogene Proteins)
0 (Proto-Oncogene Proteins)
126469-30-5 (Lcn2 protein, mouse)
E1UOL152H7 (Iron)
EC 1.14.14.18 (Heme Oxygenase (Decyclizing))
EC 1.14.14.18 (Hmox1 protein, rat)
تواريخ الأحداث: Date Created: 20140524 Date Completed: 20150608 Latest Revision: 20220410
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4158684
DOI: 10.1038/cdd.2014.68
PMID: 24853299
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5403
DOI:10.1038/cdd.2014.68