Neuroprotective and anti‐apoptotic effects of liraglutide on SH‐SY5Y cells exposed to methylglyoxal stress
Glucagon‐like peptide 1 (GLP‐1) is a growth factor that has demonstrated neuroprotective properties in a range of studies. In an APPswe/PS1ΔE9 mouse model of Alzheimer's disease (AD), we previously found protective effects on memory formation, synaptic plasticity, synapse survival and a reducti...
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| Veröffentlicht in: | Journal of neurochemistry 2014-02, Vol.128 (3), p.459-471 |
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| description | Glucagon‐like peptide 1 (GLP‐1) is a growth factor that has demonstrated neuroprotective properties in a range of studies. In an APPswe/PS1ΔE9 mouse model of Alzheimer's disease (AD), we previously found protective effects on memory formation, synaptic plasticity, synapse survival and a reduction of amyloid synthesis and plaque load in the brain. Here, we analyse the neuroprotective properties of the GLP‐1 analogue liraglutide in human neuroblastoma cell line SH‐SY5Y during methyl glyoxal stress. We show for the first time that cell viability was enhanced by liraglutide (XTT assay) in a dose‐dependent way, while cytotoxicity (LDH assay) and apoptosis were reduced. Expression of the pro‐survival Mcl1 signaling protein was increased, as was activation of cell survival kinases Akt, MEK1/2 and the transcription factor p90RSK. Liraglutide also decreased pro‐apoptotic Bax and Bik expression. In addition, the membrane potential and the influx of calcium into the cell were enhanced by liraglutide. GLP‐1 receptor expression was also increased by the drug. The results demonstrate a range of growth factor‐related cytoprotective processes induced by liraglutide, which is currently on the market as a treatment for type 2 diabetes (Victoza®). It is also tested in clinical trials in patients with Alzheimer disease.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide. |
| doi_str_mv | 10.1111/jnc.12469 |
| format | Article |
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We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/jnc.12469</identifier><identifier>PMID: 24112036</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>AKT protein ; Alzheimer's disease ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; bcl-2-Associated X Protein - metabolism ; Blotting, Western ; Brain ; Calcium - metabolism ; Caspase 3 - metabolism ; Cell Line ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cells ; Glucagon-Like Peptide 1 - analogs & derivatives ; Glucagon-Like Peptide 1 - pharmacology ; Glucagon-Like Peptide-1 Receptor ; Humans ; Hypoglycemic Agents - pharmacology ; Immunohistochemistry ; incretins ; insulin ; Liraglutide ; Membrane Potentials ; Membrane Proteins - metabolism ; Mitogen-Activated Protein Kinases - metabolism ; neurodegeneration ; neuroprotection ; Neuroprotective Agents ; Oncogene Protein v-akt - metabolism ; Peptides ; Pyruvaldehyde - toxicity ; Receptors, Glucagon - biosynthesis ; Receptors, Glucagon - genetics ; Stress analysis ; Stress, Physiological - drug effects</subject><ispartof>Journal of neurochemistry, 2014-02, Vol.128 (3), p.459-471</ispartof><rights>2013 International Society for Neurochemistry</rights><rights>2013 International Society for Neurochemistry.</rights><rights>Copyright © 2014 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjnc.12469$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjnc.12469$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24112036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sharma, Mohit K.</creatorcontrib><creatorcontrib>Jalewa, Jaishree</creatorcontrib><creatorcontrib>Hölscher, Christian</creatorcontrib><title>Neuroprotective and anti‐apoptotic effects of liraglutide on SH‐SY5Y cells exposed to methylglyoxal stress</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Glucagon‐like peptide 1 (GLP‐1) is a growth factor that has demonstrated neuroprotective properties in a range of studies. In an APPswe/PS1ΔE9 mouse model of Alzheimer's disease (AD), we previously found protective effects on memory formation, synaptic plasticity, synapse survival and a reduction of amyloid synthesis and plaque load in the brain. Here, we analyse the neuroprotective properties of the GLP‐1 analogue liraglutide in human neuroblastoma cell line SH‐SY5Y during methyl glyoxal stress. We show for the first time that cell viability was enhanced by liraglutide (XTT assay) in a dose‐dependent way, while cytotoxicity (LDH assay) and apoptosis were reduced. Expression of the pro‐survival Mcl1 signaling protein was increased, as was activation of cell survival kinases Akt, MEK1/2 and the transcription factor p90RSK. Liraglutide also decreased pro‐apoptotic Bax and Bik expression. In addition, the membrane potential and the influx of calcium into the cell were enhanced by liraglutide. GLP‐1 receptor expression was also increased by the drug. The results demonstrate a range of growth factor‐related cytoprotective processes induced by liraglutide, which is currently on the market as a treatment for type 2 diabetes (Victoza®). It is also tested in clinical trials in patients with Alzheimer disease.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.</description><subject>AKT protein</subject><subject>Alzheimer's disease</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Blotting, Western</subject><subject>Brain</subject><subject>Calcium - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cells</subject><subject>Glucagon-Like Peptide 1 - analogs & derivatives</subject><subject>Glucagon-Like Peptide 1 - pharmacology</subject><subject>Glucagon-Like Peptide-1 Receptor</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Immunohistochemistry</subject><subject>incretins</subject><subject>insulin</subject><subject>Liraglutide</subject><subject>Membrane Potentials</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>neurodegeneration</subject><subject>neuroprotection</subject><subject>Neuroprotective Agents</subject><subject>Oncogene Protein v-akt - metabolism</subject><subject>Peptides</subject><subject>Pyruvaldehyde - toxicity</subject><subject>Receptors, Glucagon - biosynthesis</subject><subject>Receptors, Glucagon - genetics</subject><subject>Stress analysis</subject><subject>Stress, Physiological - drug effects</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9OwzAMxiMEgjE48AIoEhcuZXGSZusRTfwVggNw2KlKW3d0yprSpMBuPALPyJOQscGBE5YsW_JPlj9_hBwAO4EQg1mdnwCXKtkgPZBDiCTEySbpMcZ5JJjkO2TXuRljoKSCbbLDJQBnQvVIfYtda5vWesx99YJU10VIX32-f-jGNt76KqdYlmHsqC2pqVo9NZ2vCqS2pveXAbyfxBOaozGO4ltjHRbUWzpH_7QwU7Owb9pQ51t0bo9sldo43F_XPnk8P3sYX0Y3dxdX49ObaCaDjKjAEQAbZjwURJ7IrNQSVKmEBCbiYVayYaJRZFqLUmmWyILloyyJY8Y1ZrHok-PV3qDsuUPn03nllhfqGm3nUpCJGo1UrMR_UGAKElhuPfqDzmzX1kHIkmJKxFLyQB2uqS6bY5E2bTXX7SL9eXoABivgtTK4-J0DS5dupsHN9NvN9Pp2_N2IL9DgkxE</recordid><startdate>201402</startdate><enddate>201402</enddate><creator>Sharma, Mohit K.</creator><creator>Jalewa, Jaishree</creator><creator>Hölscher, Christian</creator><general>Blackwell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201402</creationdate><title>Neuroprotective and anti‐apoptotic effects of liraglutide on SH‐SY5Y cells exposed to methylglyoxal stress</title><author>Sharma, Mohit K. ; Jalewa, Jaishree ; Hölscher, Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j4469-de81107b2811ee294bfa416f63410357bf079ae3baa3f6a094d0c8b95502aeb53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>AKT protein</topic><topic>Alzheimer's disease</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Blotting, Western</topic><topic>Brain</topic><topic>Calcium - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Line</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cells</topic><topic>Glucagon-Like Peptide 1 - analogs & derivatives</topic><topic>Glucagon-Like Peptide 1 - pharmacology</topic><topic>Glucagon-Like Peptide-1 Receptor</topic><topic>Humans</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Immunohistochemistry</topic><topic>incretins</topic><topic>insulin</topic><topic>Liraglutide</topic><topic>Membrane Potentials</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>neurodegeneration</topic><topic>neuroprotection</topic><topic>Neuroprotective Agents</topic><topic>Oncogene Protein v-akt - metabolism</topic><topic>Peptides</topic><topic>Pyruvaldehyde - toxicity</topic><topic>Receptors, Glucagon - biosynthesis</topic><topic>Receptors, Glucagon - genetics</topic><topic>Stress analysis</topic><topic>Stress, Physiological - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sharma, Mohit K.</creatorcontrib><creatorcontrib>Jalewa, Jaishree</creatorcontrib><creatorcontrib>Hölscher, Christian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sharma, Mohit K.</au><au>Jalewa, Jaishree</au><au>Hölscher, Christian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective and anti‐apoptotic effects of liraglutide on SH‐SY5Y cells exposed to methylglyoxal stress</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2014-02</date><risdate>2014</risdate><volume>128</volume><issue>3</issue><spage>459</spage><epage>471</epage><pages>459-471</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><abstract>Glucagon‐like peptide 1 (GLP‐1) is a growth factor that has demonstrated neuroprotective properties in a range of studies. In an APPswe/PS1ΔE9 mouse model of Alzheimer's disease (AD), we previously found protective effects on memory formation, synaptic plasticity, synapse survival and a reduction of amyloid synthesis and plaque load in the brain. Here, we analyse the neuroprotective properties of the GLP‐1 analogue liraglutide in human neuroblastoma cell line SH‐SY5Y during methyl glyoxal stress. We show for the first time that cell viability was enhanced by liraglutide (XTT assay) in a dose‐dependent way, while cytotoxicity (LDH assay) and apoptosis were reduced. Expression of the pro‐survival Mcl1 signaling protein was increased, as was activation of cell survival kinases Akt, MEK1/2 and the transcription factor p90RSK. Liraglutide also decreased pro‐apoptotic Bax and Bik expression. In addition, the membrane potential and the influx of calcium into the cell were enhanced by liraglutide. GLP‐1 receptor expression was also increased by the drug. The results demonstrate a range of growth factor‐related cytoprotective processes induced by liraglutide, which is currently on the market as a treatment for type 2 diabetes (Victoza®). It is also tested in clinical trials in patients with Alzheimer disease.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.
We investigated the neuroprotective properties of the GLP‐1 analogue liraglutide in SH‐SY5Y cells during methyl glyoxal stress. Cell survival was enhanced, while cytotoxicity and apoptosis was reduced. Expression of the pro‐survival Mcl1 signaling protein, activation of Akt, MEK1/2 and the transcription factor p90RSK was increased. Pro‐apoptotic Bax and Bik expression was reduced, and the influx of calcium into the cell was normalised. The results demonstrate a range of growth factor related cytoprotective processes induced by the drug liraglutide.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24112036</pmid><doi>10.1111/jnc.12469</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AKT protein Alzheimer's disease Apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins - metabolism bcl-2-Associated X Protein - metabolism Blotting, Western Brain Calcium - metabolism Caspase 3 - metabolism Cell Line Cell Proliferation - drug effects Cell Survival - drug effects Cells Glucagon-Like Peptide 1 - analogs & derivatives Glucagon-Like Peptide 1 - pharmacology Glucagon-Like Peptide-1 Receptor Humans Hypoglycemic Agents - pharmacology Immunohistochemistry incretins insulin Liraglutide Membrane Potentials Membrane Proteins - metabolism Mitogen-Activated Protein Kinases - metabolism neurodegeneration neuroprotection Neuroprotective Agents Oncogene Protein v-akt - metabolism Peptides Pyruvaldehyde - toxicity Receptors, Glucagon - biosynthesis Receptors, Glucagon - genetics Stress analysis Stress, Physiological - drug effects |
| title | Neuroprotective and anti‐apoptotic effects of liraglutide on SH‐SY5Y cells exposed to methylglyoxal stress |
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