The Adiponectin Homolog Osmotin Enhances Neurite Outgrowth and Synaptic Complexity via AdipoR1/NgR1 Signaling in Alzheimer’s Disease
Alzheimer’s disease is a major neurodegenerative disease characterized by memory loss and cognitive deficits. Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer’s disease mice. Several lines of evidence have sug...
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| Veröffentlicht in: | Molecular neurobiology 2018-08, Vol.55 (8), p.6673-6686 |
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| creator | Yoon, Gwangho Shah, Shahid Ali Ali, Tahir Kim, Myeong Ok |
| description | Alzheimer’s disease is a major neurodegenerative disease characterized by memory loss and cognitive deficits. Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer’s disease mice. Several lines of evidence have suggested that Nogo-A and the Nogo-66 receptor 1 (NgR1), which form a complex that inhibits long-term potentiation and cognitive function, might be associated with the adiponectin receptor 1 (AdipoR1), which is a receptor for osmotin. Here, we explore whether osmotin’s effects on long-term potentiation and memory function are associated with NgR1 signaling via AdipoR1 in Alzheimer’s disease. Osmotin reduced the expression of NgR1 without affecting Nogo-A expression. Furthermore, osmotin inhibited NgR1 signaling by prohibiting the formation of the Nogo-A and NgR1 ligand-receptor complex, resulting in enhanced neurite outgrowth; these effects disappeared in the presence of AdipoR1 interference. In addition, osmotin increased the expression of the pre- and postsynaptic markers synaptophysin and PSD-95, as well as the activation of the memory-associated markers AMPA receptor and CREB; these effects occurred in an AdipoR1- and NgR1-dependent manner. Osmotin was also found to enhance dendritic complexity and spine density in the hippocampal region of Alzheimer’s disease mouse brains. These results suggest that osmotin can enhance neurite outgrowth and synaptic complexity through AdipoR1 and NgR1 signaling, implying that osmotin might be an effective therapeutic agent for Alzheimer’s disease and that AdipoR1 might be a crucial therapeutic target for neurodegenerative diseases such as Alzheimer’s. |
| doi_str_mv | 10.1007/s12035-017-0847-1 |
| format | Article |
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Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer’s disease mice. Several lines of evidence have suggested that Nogo-A and the Nogo-66 receptor 1 (NgR1), which form a complex that inhibits long-term potentiation and cognitive function, might be associated with the adiponectin receptor 1 (AdipoR1), which is a receptor for osmotin. Here, we explore whether osmotin’s effects on long-term potentiation and memory function are associated with NgR1 signaling via AdipoR1 in Alzheimer’s disease. Osmotin reduced the expression of NgR1 without affecting Nogo-A expression. Furthermore, osmotin inhibited NgR1 signaling by prohibiting the formation of the Nogo-A and NgR1 ligand-receptor complex, resulting in enhanced neurite outgrowth; these effects disappeared in the presence of AdipoR1 interference. In addition, osmotin increased the expression of the pre- and postsynaptic markers synaptophysin and PSD-95, as well as the activation of the memory-associated markers AMPA receptor and CREB; these effects occurred in an AdipoR1- and NgR1-dependent manner. Osmotin was also found to enhance dendritic complexity and spine density in the hippocampal region of Alzheimer’s disease mouse brains. These results suggest that osmotin can enhance neurite outgrowth and synaptic complexity through AdipoR1 and NgR1 signaling, implying that osmotin might be an effective therapeutic agent for Alzheimer’s disease and that AdipoR1 might be a crucial therapeutic target for neurodegenerative diseases such as Alzheimer’s.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0847-1</identifier><identifier>PMID: 29335844</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adiponectin ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Animals ; Axonogenesis ; Biomarkers - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Brain - pathology ; Cell Biology ; Cell Line, Tumor ; Cognitive ability ; Cyclic AMP response element-binding protein ; Dendritic spines ; Disease ; Disease Models, Animal ; Hippocampus ; Humans ; Long-term potentiation ; Male ; Memory ; Memory - drug effects ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurobiology ; Neurodegenerative diseases ; Neurology ; Neuronal Outgrowth - drug effects ; Neurosciences ; Nogo protein ; Nogo Proteins - genetics ; Nogo Proteins - metabolism ; Nogo Receptor 1 - metabolism ; Osmotin ; Plant Proteins - pharmacology ; Postsynaptic density proteins ; Receptors, Adiponectin - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction ; Spine ; Synapses - drug effects ; Synapses - metabolism ; Synaptophysin ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors</subject><ispartof>Molecular neurobiology, 2018-08, Vol.55 (8), p.6673-6686</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2018</rights><rights>Molecular Neurobiology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-78299adc63358ec69cb2278fd3056d4ab0e1de2c6b6ae7769825a322cb3b2a2d3</citedby><cites>FETCH-LOGICAL-c442t-78299adc63358ec69cb2278fd3056d4ab0e1de2c6b6ae7769825a322cb3b2a2d3</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/s12035-017-0847-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0847-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27911,27912,41475,42544,51306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29335844$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoon, Gwangho</creatorcontrib><creatorcontrib>Shah, Shahid Ali</creatorcontrib><creatorcontrib>Ali, Tahir</creatorcontrib><creatorcontrib>Kim, Myeong Ok</creatorcontrib><title>The Adiponectin Homolog Osmotin Enhances Neurite Outgrowth and Synaptic Complexity via AdipoR1/NgR1 Signaling in Alzheimer’s Disease</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Alzheimer’s disease is a major neurodegenerative disease characterized by memory loss and cognitive deficits. Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer’s disease mice. Several lines of evidence have suggested that Nogo-A and the Nogo-66 receptor 1 (NgR1), which form a complex that inhibits long-term potentiation and cognitive function, might be associated with the adiponectin receptor 1 (AdipoR1), which is a receptor for osmotin. Here, we explore whether osmotin’s effects on long-term potentiation and memory function are associated with NgR1 signaling via AdipoR1 in Alzheimer’s disease. Osmotin reduced the expression of NgR1 without affecting Nogo-A expression. Furthermore, osmotin inhibited NgR1 signaling by prohibiting the formation of the Nogo-A and NgR1 ligand-receptor complex, resulting in enhanced neurite outgrowth; these effects disappeared in the presence of AdipoR1 interference. In addition, osmotin increased the expression of the pre- and postsynaptic markers synaptophysin and PSD-95, as well as the activation of the memory-associated markers AMPA receptor and CREB; these effects occurred in an AdipoR1- and NgR1-dependent manner. Osmotin was also found to enhance dendritic complexity and spine density in the hippocampal region of Alzheimer’s disease mouse brains. 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metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Axonogenesis</topic><topic>Biomarkers - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - pathology</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cognitive ability</topic><topic>Cyclic AMP response element-binding protein</topic><topic>Dendritic spines</topic><topic>Disease</topic><topic>Disease Models, Animal</topic><topic>Hippocampus</topic><topic>Humans</topic><topic>Long-term potentiation</topic><topic>Male</topic><topic>Memory</topic><topic>Memory - drug effects</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neurobiology</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neuronal Outgrowth - drug effects</topic><topic>Neurosciences</topic><topic>Nogo protein</topic><topic>Nogo Proteins - genetics</topic><topic>Nogo Proteins - metabolism</topic><topic>Nogo Receptor 1 - metabolism</topic><topic>Osmotin</topic><topic>Plant Proteins - pharmacology</topic><topic>Postsynaptic density proteins</topic><topic>Receptors, Adiponectin - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>Spine</topic><topic>Synapses - drug effects</topic><topic>Synapses - metabolism</topic><topic>Synaptophysin</topic><topic>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</topic><topic>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoon, Gwangho</creatorcontrib><creatorcontrib>Shah, Shahid Ali</creatorcontrib><creatorcontrib>Ali, Tahir</creatorcontrib><creatorcontrib>Kim, Myeong Ok</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoon, Gwangho</au><au>Shah, Shahid Ali</au><au>Ali, Tahir</au><au>Kim, Myeong Ok</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Adiponectin Homolog Osmotin Enhances Neurite Outgrowth and Synaptic Complexity via AdipoR1/NgR1 Signaling in Alzheimer’s Disease</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018-08-01</date><risdate>2018</risdate><volume>55</volume><issue>8</issue><spage>6673</spage><epage>6686</epage><pages>6673-6686</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Alzheimer’s disease is a major neurodegenerative disease characterized by memory loss and cognitive deficits. Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer’s disease mice. Several lines of evidence have suggested that Nogo-A and the Nogo-66 receptor 1 (NgR1), which form a complex that inhibits long-term potentiation and cognitive function, might be associated with the adiponectin receptor 1 (AdipoR1), which is a receptor for osmotin. Here, we explore whether osmotin’s effects on long-term potentiation and memory function are associated with NgR1 signaling via AdipoR1 in Alzheimer’s disease. Osmotin reduced the expression of NgR1 without affecting Nogo-A expression. Furthermore, osmotin inhibited NgR1 signaling by prohibiting the formation of the Nogo-A and NgR1 ligand-receptor complex, resulting in enhanced neurite outgrowth; these effects disappeared in the presence of AdipoR1 interference. In addition, osmotin increased the expression of the pre- and postsynaptic markers synaptophysin and PSD-95, as well as the activation of the memory-associated markers AMPA receptor and CREB; these effects occurred in an AdipoR1- and NgR1-dependent manner. Osmotin was also found to enhance dendritic complexity and spine density in the hippocampal region of Alzheimer’s disease mouse brains. These results suggest that osmotin can enhance neurite outgrowth and synaptic complexity through AdipoR1 and NgR1 signaling, implying that osmotin might be an effective therapeutic agent for Alzheimer’s disease and that AdipoR1 might be a crucial therapeutic target for neurodegenerative diseases such as Alzheimer’s.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29335844</pmid><doi>10.1007/s12035-017-0847-1</doi><tpages>14</tpages></addata></record> |
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| ispartof | Molecular neurobiology, 2018-08, Vol.55 (8), p.6673-6686 |
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| subjects | Adiponectin Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - metabolism Animals Axonogenesis Biomarkers - metabolism Biomedical and Life Sciences Biomedicine Brain - pathology Cell Biology Cell Line, Tumor Cognitive ability Cyclic AMP response element-binding protein Dendritic spines Disease Disease Models, Animal Hippocampus Humans Long-term potentiation Male Memory Memory - drug effects Mice, Inbred C57BL Mice, Transgenic Neurobiology Neurodegenerative diseases Neurology Neuronal Outgrowth - drug effects Neurosciences Nogo protein Nogo Proteins - genetics Nogo Proteins - metabolism Nogo Receptor 1 - metabolism Osmotin Plant Proteins - pharmacology Postsynaptic density proteins Receptors, Adiponectin - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction Spine Synapses - drug effects Synapses - metabolism Synaptophysin α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors |
| title | The Adiponectin Homolog Osmotin Enhances Neurite Outgrowth and Synaptic Complexity via AdipoR1/NgR1 Signaling in Alzheimer’s Disease |
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