DNA polymerase-β mediates the neurogenic effect of β-amyloid protein in cultured subventricular zone neurospheres (701 views)
Journal Of Neuroscience Research (ISSN: 0360-4012), 2012 Mar; 90(3): 559-567.
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Paper type: Journal Article, Research Support, N. I. H. , Extramural, Non-U. S. Gov'T,
Impact factor: 2.974, 5-year impact factor: 3.018
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84855876064&partnerID=40&md5=17d41a5e6defbf9f531176781415a743
Keywords: β-Amyloid, Alzheimer, S Disease, Dna Polymerase-β, Neural Stem Cell, Neurogenesis, Neurosphere, Amyloid Beta Protein, Amyloid Beta Protein[1-42], Dna Directed Dna Polymerase Beta, Microtubule Associated Protein 2, Nestin, Animal Cell, Article, Brain Development, Cell Culture, Cell Cycle Arrest, Cell Differentiation, Cell Maturation, Cell Proliferation, Controlled Study, Gene Expression, Gene Silencing, Mouse, Nerve Cell, Nervous System Development, Neuroblast, Nonhuman, Priority Journal, Subventricular Zone, Amyloid Beta-Peptides, Cell Cycle Checkpoints, Cerebral Ventricles, Amyloid Beta-Peptides Metabolism Pharmacology, Cell Cycle Checkpoints Drug Effects Physiology, Cell Proliferation Drug Effects, Cerebral Ventricles Cytology Metabolism, Dna Polymerase Beta Metabolism Pharmacology, Neurogenesis Drug Effects Physiology, Neurons Cytology Drug Effects Metabolism, Amyloid Beta Protein [1-42],
Affiliations:
*** IBB - CNR ***
Department of Cell Biology and Human Anatomy, Institute for Pediatric Regenerative Medicine, School of Medicine, University of California, Davis, CA, United States
Department of Pharmaceutical Sciences, University of Catania, Catania, Italy
Istituto di Bioimmagini e Biostrutture, CNR, Catania, Italy
References:
Not available.
Journal Of Neuroscience Research (ISSN: 0360-4012), 2012 Mar; 90(3): 559-567.
Export to BibTeX Export to EndNote
Paper type: Journal Article, Research Support, N. I. H. , Extramural, Non-U. S. Gov'T,
Impact factor: 2.974, 5-year impact factor: 3.018
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84855876064&partnerID=40&md5=17d41a5e6defbf9f531176781415a743
Keywords: β-Amyloid, Alzheimer, S Disease, Dna Polymerase-β, Neural Stem Cell, Neurogenesis, Neurosphere, Amyloid Beta Protein, Amyloid Beta Protein[1-42], Dna Directed Dna Polymerase Beta, Microtubule Associated Protein 2, Nestin, Animal Cell, Article, Brain Development, Cell Culture, Cell Cycle Arrest, Cell Differentiation, Cell Maturation, Cell Proliferation, Controlled Study, Gene Expression, Gene Silencing, Mouse, Nerve Cell, Nervous System Development, Neuroblast, Nonhuman, Priority Journal, Subventricular Zone, Amyloid Beta-Peptides, Cell Cycle Checkpoints, Cerebral Ventricles, Amyloid Beta-Peptides Metabolism Pharmacology, Cell Cycle Checkpoints Drug Effects Physiology, Cell Proliferation Drug Effects, Cerebral Ventricles Cytology Metabolism, Dna Polymerase Beta Metabolism Pharmacology, Neurogenesis Drug Effects Physiology, Neurons Cytology Drug Effects Metabolism, Amyloid Beta Protein [1-42],
Affiliations:
*** IBB - CNR ***
Department of Cell Biology and Human Anatomy, Institute for Pediatric Regenerative Medicine, School of Medicine, University of California, Davis, CA, United States
Department of Pharmaceutical Sciences, University of Catania, Catania, Italy
Istituto di Bioimmagini e Biostrutture, CNR, Catania, Italy
References:
Not available.
DNA polymerase-β mediates the neurogenic effect of β-amyloid protein in cultured subventricular zone neurospheres
β-Amyloid protein (Aβ) is thought to be responsible for neuronal apoptosis in Alzheimer's disease (AD). Paradoxically, Aβ can also promote neurogenesis, both in vitro and in vivo, by inducing neural progenitor cells (NPCs) to differentiate into neurons. However, the mechanisms of Aβ-induced neurogenesis are unknown. Here we examined the role of DNA polymerase-β (DNA pol-β), a DNA repair enzyme that is required for proper neurogenesis during brain development and is also responsible for Aβ-induced neuronal apoptosis. In neurospheres obtained from the adult mouse subventricular zone (SVZ), the knockdown of DNA pol-β or its pharmacological blockade showed that the enzyme functioned both to repress proliferation of early nestin + progenitor cells and to promote the maturation of TuJ-1 + neuronal cells. In neurospheres challenged with oligomers of synthetic Aβ 42, the expression levels of DNA pol-β were rapidly increased. DNA pol-β knockdown prevented the Aβ 42-promoted differentiation of nestin + progenitor cells into nestin +/Dlx-2 + neuroblasts. Moreover, when neurospheres were seeded to allow full differentiation of their elements, blockade of DNA pol-β prevented Aβ 42-induced differentiation of progenitors into MAP-2 + neurons. Thus, our data demonstrate that Aβ 42 arrests the proliferation of a subpopulation of nestin + cells via the induction of DNA pol-β, thereby allowing for their differentiation toward the neuronal lineage. Our findings reveal a novel role of DNA pol-β in Aβ 42-induced neurogenesis and identify DNA pol-β as a key mechanistic link between the neurogenic effect of Aβ 42 on NPCs and the proapoptotic effect of Aβ 42 on mature neurons. © 2011 Wiley Periodicals, Inc.
β-Amyloid protein (Aβ) is thought to be responsible for neuronal apoptosis in Alzheimer's disease (AD). Paradoxically, Aβ can also promote neurogenesis, both in vitro and in vivo, by inducing neural progenitor cells (NPCs) to differentiate into neurons. However, the mechanisms of Aβ-induced neurogenesis are unknown. Here we examined the role of DNA polymerase-β (DNA pol-β), a DNA repair enzyme that is required for proper neurogenesis during brain development and is also responsible for Aβ-induced neuronal apoptosis. In neurospheres obtained from the adult mouse subventricular zone (SVZ), the knockdown of DNA pol-β or its pharmacological blockade showed that the enzyme functioned both to repress proliferation of early nestin + progenitor cells and to promote the maturation of TuJ-1 + neuronal cells. In neurospheres challenged with oligomers of synthetic Aβ 42, the expression levels of DNA pol-β were rapidly increased. DNA pol-β knockdown prevented the Aβ 42-promoted differentiation of nestin + progenitor cells into nestin +/Dlx-2 + neuroblasts. Moreover, when neurospheres were seeded to allow full differentiation of their elements, blockade of DNA pol-β prevented Aβ 42-induced differentiation of progenitors into MAP-2 + neurons. Thus, our data demonstrate that Aβ 42 arrests the proliferation of a subpopulation of nestin + cells via the induction of DNA pol-β, thereby allowing for their differentiation toward the neuronal lineage. Our findings reveal a novel role of DNA pol-β in Aβ 42-induced neurogenesis and identify DNA pol-β as a key mechanistic link between the neurogenic effect of Aβ 42 on NPCs and the proapoptotic effect of Aβ 42 on mature neurons. © 2011 Wiley Periodicals, Inc.
DNA polymerase-β mediates the neurogenic effect of β-amyloid protein in cultured subventricular zone neurospheres
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DNA polymerase-β mediates the neurogenic effect of β-amyloid protein in cultured subventricular zone neurospheres
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View Export to BibTeX Export to EndNote
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Castiglione M, Calafiore M, Costa L, Sortino MA, Nicoletti F, Copani A
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Neuropharm (ISSN: 0028-3908, 1873-7064electronic, 0028-3908linking), 2008 Sep; 55(4): 560-567.
Impact Factor: 3.383
View Export to BibTeX Export to EndNote
Copani A, Guccione S, Giurato L, Caraci F, Calafiore M, Sortino MA
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Impact Factor: 4.823
View Export to BibTeX Export to EndNote
Copani A, Caraci F, Hoozemans J, Calafiore M, Sortino M, Nicoletti F
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Impact Factor: 3.078
View Export to BibTeX Export to EndNote
Giuffrida ML, Grasso G, Ruvo M, Pedone C, Saporito A, Marasco D, Pignataro B, Cascio C, Copani A, Rizzarelli E
* Abeta(25-35) And Its C- And/Or N-Blocked Derivatives: Copper Driven Structural Features And Neurotoxicity (721 views)
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Impact Factor: 3.268
View Export to BibTeX Export to EndNote
Copani A, Hoozemans JJM, Caraci F, Calafiore M, Van Haastert ES, Veerhuis R, Rozemuller AJM, Aronica E, Sortino MA, Nicoletti F
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Impact Factor: 2.117
View Export to BibTeX Export to EndNote
Calafiore M, Battaglia G, Zappal A, Trovato-Salinaro E, Caraci F, Caruso M, Vancheri C, Sortino MA, Nicoletti F, Copani A
* Progenitor cells from the adult mouse brain acquire a neuronal phenotype in response to β-amyloid (865 views)
Neurobiol Aging (ISSN: 0197-4580, 1558-1497electronic, 0197-4580linking), 2006; 27(4): 606-613.
Impact Factor: 5.599
View Export to BibTeX Export to EndNote
Marrazzo A, Caraci F, Salinaro ET, Su TP, Copani A, Ronsisvalle G
* Neuroprotective effects of sigma-1 receptor agonists against beta-amyloid-induced toxicity (700 views)
Neuroreport (ISSN: 0959-4965), 2005 Sep 1; 16(11): 1223-1226.
Impact Factor: 1.995
View Export to BibTeX Export to EndNote
Filippo C, Mariangela C, Giuseppina F, Pier Luigi C, Angelo B, Marco C, Giuseppe B, Paolo B, Ferdinando N, Agata C, Maria Angela S
* Nicergoline, a drug used for age-dependent cognitive impairment, protects cultured neurons against β-amyloid toxicity (907 views)
Brain Res (ISSN: 0006-8993), 2005; 1047(1): 30-37.
Impact Factor: 2.296
View Export to BibTeX Export to EndNote
Caricasole A, Copani A, Caraci F, Aronica E, Rozemuller AJ, Caruso A, Storto M, Gaviraghi G, Terstappen GC, Nicoletti F
* Induction of Dickkopf-1, a negative modulator of the Wnt pathway, is associated with neuronal degeneration in Alzheimer's brain (675 views)
J Neurosci (ISSN: 0270-6474, 0361-803x, 1529-2401), 2004 Jun 30; 24(26): 6021-6027.
Impact Factor: 2.384
View Export to BibTeX Export to EndNote
18 Records (18 excluding Abstracts).
Total impact factor: 83.434 (83.434 excluding Abstracts).
Total 5 year impact factor: 84.007 (84.007 excluding Abstracts).
Total impact factor: 83.434 (83.434 excluding Abstracts).
Total 5 year impact factor: 84.007 (84.007 excluding Abstracts).
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