Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation
Amyloid β (A β ) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in A β -induced neurotoxicity. We have reported that apoptosis signal-regulating...
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| Veröffentlicht in: | Cell death and differentiation 2005-01, Vol.12 (1), p.19-24 |
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| container_title | Cell death and differentiation |
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| creator | Kadowaki, H Nishitoh, H Urano, F Sadamitsu, C Matsuzawa, A Takeda, K Masutani, H Yodoi, J Urano, Y Nagano, T Ichijo, H |
| description | Amyloid
β
(A
β
) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in A
β
-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in A
β
-induced neuronal cell death. A
β
activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly,
ASK1
−/−
neurons were defective in A
β
-induced JNK activation and cell death. These results indicate that ROS-mediated ASK1 activation is a key mechanism for A
β
-induced neurotoxicity, which plays a central role in Alzheimer's disease. |
| doi_str_mv | 10.1038/sj.cdd.4401528 |
| format | Article |
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β
(A
β
) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in A
β
-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in A
β
-induced neuronal cell death. A
β
activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly,
ASK1
−/−
neurons were defective in A
β
-induced JNK activation and cell death. These results indicate that ROS-mediated ASK1 activation is a key mechanism for A
β
-induced neurotoxicity, which plays a central role in Alzheimer's disease.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/sj.cdd.4401528</identifier><identifier>PMID: 15592360</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Alzheimer Disease - etiology ; Amyloid beta-Peptides - pharmacology ; Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Cycle Analysis ; Cell Death - drug effects ; eIF-2 Kinase - metabolism ; Endoplasmic Reticulum - enzymology ; Endoplasmic Reticulum - metabolism ; Enzyme Activation - drug effects ; JNK Mitogen-Activated Protein Kinases - metabolism ; Life Sciences ; MAP Kinase Kinase Kinase 5 - genetics ; MAP Kinase Kinase Kinase 5 - metabolism ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons - cytology ; Neurons - drug effects ; Neurons - metabolism ; Nitrogen Oxides - metabolism ; original-paper ; PC12 Cells ; Peptide Fragments - pharmacology ; Protein-Serine-Threonine Kinases - metabolism ; Rats ; Reactive Oxygen Species - metabolism ; Stem Cells</subject><ispartof>Cell death and differentiation, 2005-01, Vol.12 (1), p.19-24</ispartof><rights>Springer Nature Limited 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-a151d9901ddb4744e828d7f4d40833dc8b796e49697cb4f5da8ea92888720a483</citedby><cites>FETCH-LOGICAL-c404t-a151d9901ddb4744e828d7f4d40833dc8b796e49697cb4f5da8ea92888720a483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.cdd.4401528$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.cdd.4401528$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15592360$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kadowaki, H</creatorcontrib><creatorcontrib>Nishitoh, H</creatorcontrib><creatorcontrib>Urano, F</creatorcontrib><creatorcontrib>Sadamitsu, C</creatorcontrib><creatorcontrib>Matsuzawa, A</creatorcontrib><creatorcontrib>Takeda, K</creatorcontrib><creatorcontrib>Masutani, H</creatorcontrib><creatorcontrib>Yodoi, J</creatorcontrib><creatorcontrib>Urano, Y</creatorcontrib><creatorcontrib>Nagano, T</creatorcontrib><creatorcontrib>Ichijo, H</creatorcontrib><title>Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Amyloid
β
(A
β
) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in A
β
-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in A
β
-induced neuronal cell death. A
β
activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly,
ASK1
−/−
neurons were defective in A
β
-induced JNK activation and cell death. These results indicate that ROS-mediated ASK1 activation is a key mechanism for A
β
-induced neurotoxicity, which plays a central role in Alzheimer's disease.</description><subject>Alzheimer Disease - etiology</subject><subject>Amyloid beta-Peptides - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell Death - drug effects</subject><subject>eIF-2 Kinase - metabolism</subject><subject>Endoplasmic Reticulum - enzymology</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Enzyme Activation - drug effects</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Life Sciences</subject><subject>MAP Kinase Kinase Kinase 5 - genetics</subject><subject>MAP Kinase Kinase Kinase 5 - metabolism</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Nitrogen Oxides - metabolism</subject><subject>original-paper</subject><subject>PC12 Cells</subject><subject>Peptide Fragments - pharmacology</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Stem Cells</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOwzAQRS0EolDYskResUtqJ5PEXlYVL7VSJQpry7GdNlEexU6Q-lt8CN-Eq0ZixWpGmjNXMwehO0pCSmI2c1WotA4BCE0idoauKGRpkACJz30fJyTgBLIJunauIoSkGU8v0YQmCY_ilFyh5bw51F2p8c83Lls9KONwawbbtbLGytQ11kb2O9zvbDdsd_htvQkao0vZG43nmyXFUvXll-zLrr1BF4Wsnbkd6xR9PD2-L16C1fr5dTFfBQoI9IGkCdWcE6p1DhmAYRHTWQEaCItjrVjujzTAU56pHIpES2YkjxhjWUQksHiKHk65e9t9Dsb1oind8VbZmm5wgmb-tQjAg-EJVLZzzppC7G3ZSHsQlIijPuEq4fWJUZ9fuB-Th9x_-YePvjwwOwHOj9qtsaLqButduf8ifwFkuntH</recordid><startdate>20050101</startdate><enddate>20050101</enddate><creator>Kadowaki, H</creator><creator>Nishitoh, H</creator><creator>Urano, F</creator><creator>Sadamitsu, C</creator><creator>Matsuzawa, A</creator><creator>Takeda, K</creator><creator>Masutani, H</creator><creator>Yodoi, J</creator><creator>Urano, Y</creator><creator>Nagano, T</creator><creator>Ichijo, H</creator><general>Nature Publishing Group UK</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>7TK</scope></search><sort><creationdate>20050101</creationdate><title>Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation</title><author>Kadowaki, H ; Nishitoh, H ; Urano, F ; Sadamitsu, C ; Matsuzawa, A ; Takeda, K ; Masutani, H ; Yodoi, J ; Urano, Y ; Nagano, T ; Ichijo, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-a151d9901ddb4744e828d7f4d40833dc8b796e49697cb4f5da8ea92888720a483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Alzheimer Disease - etiology</topic><topic>Amyloid beta-Peptides - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Cycle Analysis</topic><topic>Cell Death - drug effects</topic><topic>eIF-2 Kinase - metabolism</topic><topic>Endoplasmic Reticulum - enzymology</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Enzyme Activation - drug effects</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Life Sciences</topic><topic>MAP Kinase Kinase Kinase 5 - genetics</topic><topic>MAP Kinase Kinase Kinase 5 - metabolism</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Nitrogen Oxides - metabolism</topic><topic>original-paper</topic><topic>PC12 Cells</topic><topic>Peptide Fragments - pharmacology</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Rats</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Stem Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kadowaki, H</creatorcontrib><creatorcontrib>Nishitoh, H</creatorcontrib><creatorcontrib>Urano, F</creatorcontrib><creatorcontrib>Sadamitsu, C</creatorcontrib><creatorcontrib>Matsuzawa, A</creatorcontrib><creatorcontrib>Takeda, K</creatorcontrib><creatorcontrib>Masutani, H</creatorcontrib><creatorcontrib>Yodoi, J</creatorcontrib><creatorcontrib>Urano, Y</creatorcontrib><creatorcontrib>Nagano, T</creatorcontrib><creatorcontrib>Ichijo, H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kadowaki, H</au><au>Nishitoh, H</au><au>Urano, F</au><au>Sadamitsu, C</au><au>Matsuzawa, A</au><au>Takeda, K</au><au>Masutani, H</au><au>Yodoi, J</au><au>Urano, Y</au><au>Nagano, T</au><au>Ichijo, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2005-01-01</date><risdate>2005</risdate><volume>12</volume><issue>1</issue><spage>19</spage><epage>24</epage><pages>19-24</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Amyloid
β
(A
β
) is a main component of senile plaques in Alzheimer's disease and induces neuronal cell death. Reactive oxygen species (ROS), nitric oxide and endoplasmic reticulum (ER) stress have been implicated in A
β
-induced neurotoxicity. We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Here we show the involvement of ASK1 in A
β
-induced neuronal cell death. A
β
activated ASK1 mainly through production of ROS but not through ER stress in cultured neuronal cells. Importantly,
ASK1
−/−
neurons were defective in A
β
-induced JNK activation and cell death. These results indicate that ROS-mediated ASK1 activation is a key mechanism for A
β
-induced neurotoxicity, which plays a central role in Alzheimer's disease.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15592360</pmid><doi>10.1038/sj.cdd.4401528</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_proquest_miscellaneous_17360244 |
| source | MEDLINE; SpringerLink Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Alzheimer Disease - etiology Amyloid beta-Peptides - pharmacology Animals Apoptosis Biochemistry Biomedical and Life Sciences Cell Biology Cell Cycle Analysis Cell Death - drug effects eIF-2 Kinase - metabolism Endoplasmic Reticulum - enzymology Endoplasmic Reticulum - metabolism Enzyme Activation - drug effects JNK Mitogen-Activated Protein Kinases - metabolism Life Sciences MAP Kinase Kinase Kinase 5 - genetics MAP Kinase Kinase Kinase 5 - metabolism Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Knockout Neurons - cytology Neurons - drug effects Neurons - metabolism Nitrogen Oxides - metabolism original-paper PC12 Cells Peptide Fragments - pharmacology Protein-Serine-Threonine Kinases - metabolism Rats Reactive Oxygen Species - metabolism Stem Cells |
| title | Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation |
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