Acceleration of the Development of Alzheimer’s Disease in Amyloid Beta-Infused Peroxiredoxin 6 Overexpression Transgenic Mice
The amyloid beta (Aβ) peptide in the brains of patients with Alzheimer’s disease (AD) is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Peroxiredoxin 6 (Prdx6) is an antioxidant protein and could act as a cytoprotective protein. However, the role of Prdx6 in neurodeg...
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| Veröffentlicht in: | Molecular neurobiology 2013-12, Vol.48 (3), p.941-951 |
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| creator | Yun, Hyung-Mun Jin, Peng Han, Jin-Yi Lee, Moon-Soon Han, Sang-Bae Oh, Ki-Wan Hong, Sung-Han Jung, Eun-Yong Hong, Jin Tae |
| description | The amyloid beta (Aβ) peptide in the brains of patients with Alzheimer’s disease (AD) is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Peroxiredoxin 6 (Prdx6) is an antioxidant protein and could act as a cytoprotective protein. However, the role of Prdx6 in neurodegenerative disease has not been studied. Thus, the roles and action mechanisms in the development of AD were examined. Aβ
1–42
-induced memory impairment in Prdx6 transgenic mice was worse than C57BL/6 mice, and the expression of amyloid precursor protein cleavage, C99, β-site APP-cleaving enzyme 1, inducible nitric oxide synthase, and cyclooxygenase-2 was greatly increased. In addition, the astrocytes and microglia cells of Aβ-infused Prdx6 transgenic mice were more activated, and Aβ also significantly increased lipid peroxidation and protein carbonyl levels, but decreased glutathione levels. Furthermore, we found that translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus was increased in Aβ-infused Prdx6 transgenic mice. These results suggest that the overexpression of Prdx6 could accelerate the development of AD through increased amyloidogenesis through independent PLA2 activation and Nrf2 transcription. |
| doi_str_mv | 10.1007/s12035-013-8479-6 |
| format | Article |
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1–42
-induced memory impairment in Prdx6 transgenic mice was worse than C57BL/6 mice, and the expression of amyloid precursor protein cleavage, C99, β-site APP-cleaving enzyme 1, inducible nitric oxide synthase, and cyclooxygenase-2 was greatly increased. In addition, the astrocytes and microglia cells of Aβ-infused Prdx6 transgenic mice were more activated, and Aβ also significantly increased lipid peroxidation and protein carbonyl levels, but decreased glutathione levels. Furthermore, we found that translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus was increased in Aβ-infused Prdx6 transgenic mice. These results suggest that the overexpression of Prdx6 could accelerate the development of AD through increased amyloidogenesis through independent PLA2 activation and Nrf2 transcription.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-013-8479-6</identifier><identifier>PMID: 23771816</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Alzheimer Disease - complications ; Alzheimer Disease - enzymology ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid beta-Peptides - toxicity ; Amyloid Precursor Protein Secretases - metabolism ; Animals ; Aspartic Acid Endopeptidases - metabolism ; Astrocytes - drug effects ; Astrocytes - enzymology ; Astrocytes - pathology ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cyclooxygenase 2 - metabolism ; Disease Progression ; Female ; Gene expression ; Glutathione - metabolism ; Lipid Peroxidation - drug effects ; Memory Disorders - complications ; Memory Disorders - enzymology ; Memory Disorders - pathology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia - drug effects ; Microglia - enzymology ; Microglia - pathology ; Neurobiology ; Neurodegeneration ; Neurology ; Neurosciences ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Nitric Oxide Synthase Type II - metabolism ; Oxidative Stress - drug effects ; Pathogenesis ; Peroxiredoxin VI - metabolism ; Phospholipases A2 - metabolism ; Protein Carbonylation - drug effects ; Proteins ; Transcription, Genetic - drug effects ; Transgenic animals</subject><ispartof>Molecular neurobiology, 2013-12, Vol.48 (3), p.941-951</ispartof><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-b368de27834a76da2d0e5f4ef4bad815adb86a0652a19e850ecef442f37fda003</citedby><cites>FETCH-LOGICAL-c372t-b368de27834a76da2d0e5f4ef4bad815adb86a0652a19e850ecef442f37fda003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-013-8479-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-013-8479-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23771816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yun, Hyung-Mun</creatorcontrib><creatorcontrib>Jin, Peng</creatorcontrib><creatorcontrib>Han, Jin-Yi</creatorcontrib><creatorcontrib>Lee, Moon-Soon</creatorcontrib><creatorcontrib>Han, Sang-Bae</creatorcontrib><creatorcontrib>Oh, Ki-Wan</creatorcontrib><creatorcontrib>Hong, Sung-Han</creatorcontrib><creatorcontrib>Jung, Eun-Yong</creatorcontrib><creatorcontrib>Hong, Jin Tae</creatorcontrib><title>Acceleration of the Development of Alzheimer’s Disease in Amyloid Beta-Infused Peroxiredoxin 6 Overexpression Transgenic Mice</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>The amyloid beta (Aβ) peptide in the brains of patients with Alzheimer’s disease (AD) is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Peroxiredoxin 6 (Prdx6) is an antioxidant protein and could act as a cytoprotective protein. However, the role of Prdx6 in neurodegenerative disease has not been studied. Thus, the roles and action mechanisms in the development of AD were examined. Aβ
1–42
-induced memory impairment in Prdx6 transgenic mice was worse than C57BL/6 mice, and the expression of amyloid precursor protein cleavage, C99, β-site APP-cleaving enzyme 1, inducible nitric oxide synthase, and cyclooxygenase-2 was greatly increased. In addition, the astrocytes and microglia cells of Aβ-infused Prdx6 transgenic mice were more activated, and Aβ also significantly increased lipid peroxidation and protein carbonyl levels, but decreased glutathione levels. Furthermore, we found that translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus was increased in Aβ-infused Prdx6 transgenic mice. These results suggest that the overexpression of Prdx6 could accelerate the development of AD through increased amyloidogenesis through independent PLA2 activation and Nrf2 transcription.</description><subject>Alzheimer Disease - complications</subject><subject>Alzheimer Disease - enzymology</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - toxicity</subject><subject>Amyloid Precursor Protein Secretases - metabolism</subject><subject>Animals</subject><subject>Aspartic Acid Endopeptidases - metabolism</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - enzymology</subject><subject>Astrocytes - pathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gene expression</subject><subject>Glutathione - metabolism</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Memory Disorders - complications</subject><subject>Memory Disorders - enzymology</subject><subject>Memory Disorders - pathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microglia - drug effects</subject><subject>Microglia - enzymology</subject><subject>Microglia - pathology</subject><subject>Neurobiology</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Pathogenesis</subject><subject>Peroxiredoxin VI - metabolism</subject><subject>Phospholipases A2 - metabolism</subject><subject>Protein Carbonylation - drug effects</subject><subject>Proteins</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transgenic animals</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kMtOwzAQRS0EouXxAWyQJdYGPxLbWZbylECwgLXlxhNwlTjFTitgA7_B7_ElpCogNmxmpLl37pUOQnuMHjJK1VFinIqcUCaIzlRB5BoasjwvCGOar6Mh1YUgSmZ6gLZSmlLKOaNqEw24UIppJofobVSWUEO0nW8DbivcPQI-gQXU7ayB0C1Po_r1EXwD8fP9I-ETn8AmwD7gUfNSt97hY-gsuQzVPIHDtxDbZx_B9TNgiW8WEOF5FiGlZcVdtCE9QPAlvvYl7KCNytYJdr_3Nro_O70bX5Crm_PL8eiKlELxjkyE1A640iKzSjrLHYW8yqDKJtZplls30dJSmXPLCtA5hbLXMl4JVTlLqdhGB6vcWWyf5pA6M23nMfSVhmWZLiQVTPQutnKVsU0pQmVm0Tc2vhhGzRK5WSE3PXKzRG5k_7P_nTyfNOB-P34Y9wa-MqReCg8Q_1T_m_oFbSaO2Q</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Yun, Hyung-Mun</creator><creator>Jin, Peng</creator><creator>Han, Jin-Yi</creator><creator>Lee, Moon-Soon</creator><creator>Han, Sang-Bae</creator><creator>Oh, Ki-Wan</creator><creator>Hong, Sung-Han</creator><creator>Jung, Eun-Yong</creator><creator>Hong, Jin Tae</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20131201</creationdate><title>Acceleration of the Development of Alzheimer’s Disease in Amyloid Beta-Infused Peroxiredoxin 6 Overexpression Transgenic Mice</title><author>Yun, Hyung-Mun ; Jin, Peng ; Han, Jin-Yi ; Lee, Moon-Soon ; Han, Sang-Bae ; Oh, Ki-Wan ; Hong, Sung-Han ; Jung, Eun-Yong ; Hong, Jin Tae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-b368de27834a76da2d0e5f4ef4bad815adb86a0652a19e850ecef442f37fda003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alzheimer Disease - 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Peroxiredoxin 6 (Prdx6) is an antioxidant protein and could act as a cytoprotective protein. However, the role of Prdx6 in neurodegenerative disease has not been studied. Thus, the roles and action mechanisms in the development of AD were examined. Aβ
1–42
-induced memory impairment in Prdx6 transgenic mice was worse than C57BL/6 mice, and the expression of amyloid precursor protein cleavage, C99, β-site APP-cleaving enzyme 1, inducible nitric oxide synthase, and cyclooxygenase-2 was greatly increased. In addition, the astrocytes and microglia cells of Aβ-infused Prdx6 transgenic mice were more activated, and Aβ also significantly increased lipid peroxidation and protein carbonyl levels, but decreased glutathione levels. Furthermore, we found that translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) to the nucleus was increased in Aβ-infused Prdx6 transgenic mice. These results suggest that the overexpression of Prdx6 could accelerate the development of AD through increased amyloidogenesis through independent PLA2 activation and Nrf2 transcription.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23771816</pmid><doi>10.1007/s12035-013-8479-6</doi><tpages>11</tpages></addata></record> |
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| ispartof | Molecular neurobiology, 2013-12, Vol.48 (3), p.941-951 |
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| subjects | Alzheimer Disease - complications Alzheimer Disease - enzymology Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - toxicity Amyloid Precursor Protein Secretases - metabolism Animals Aspartic Acid Endopeptidases - metabolism Astrocytes - drug effects Astrocytes - enzymology Astrocytes - pathology Biomedical and Life Sciences Biomedicine Cell Biology Cyclooxygenase 2 - metabolism Disease Progression Female Gene expression Glutathione - metabolism Lipid Peroxidation - drug effects Memory Disorders - complications Memory Disorders - enzymology Memory Disorders - pathology Mice Mice, Inbred C57BL Mice, Transgenic Microglia - drug effects Microglia - enzymology Microglia - pathology Neurobiology Neurodegeneration Neurology Neurosciences NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Nitric Oxide Synthase Type II - metabolism Oxidative Stress - drug effects Pathogenesis Peroxiredoxin VI - metabolism Phospholipases A2 - metabolism Protein Carbonylation - drug effects Proteins Transcription, Genetic - drug effects Transgenic animals |
| title | Acceleration of the Development of Alzheimer’s Disease in Amyloid Beta-Infused Peroxiredoxin 6 Overexpression Transgenic Mice |
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