Neuroprotective effects of stanniocalcin 2 following kainic acid-induced hippocampal degeneration in ICR mice
▶ STC2 attenuates KA-induced neuronal death. ▶ STC2 attenuates KA-induced microglial activation. ▶ STC2 attenuates KA-induced HO-1 expression in the glial cells. ▶ STC2 inhibits expression levels of NO, TNF-α, and IL-1β in LPS-stimulated BV2 cells. Stanniocalcin 2 (STC2), the paralog of STC1, has be...
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| Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2010-11, Vol.31 (11), p.2094-2099 |
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| creator | Byun, Jong-Seon Lee, Jae-Won Kim, Su Young Kwon, Kwang Jun Sohn, Jong-Hee Lee, Kyunyoung Oh, Dahlkyun Kim, Sung-Soo Chun, Wanjoo Lee, Hee Jae |
| description | ▶ STC2 attenuates KA-induced neuronal death. ▶ STC2 attenuates KA-induced microglial activation. ▶ STC2 attenuates KA-induced HO-1 expression in the glial cells. ▶ STC2 inhibits expression levels of NO, TNF-α, and IL-1β in LPS-stimulated BV2 cells.
Stanniocalcin 2 (STC2), the paralog of STC1, has been shown to act as a novel target of the mammalian unfolded protein response. We investigated the potential neuroprotective actions of STC2 against kainic acid toxicity in the hippocampus of ICR mice. STC2-treated mice experienced less neuronal cell loss in the CA3 area of the hippocampus. Also, microglial activation and heme oxygenase 1 expression were attenuated in the hippocampus of STC2-treated mice. To confirm whether STC2 regulates microglial activation directly, nitric oxide levels were measured in BV2 cells cultured with and without 10
nM STC2. STC2 decreased the level of nitric oxide induced by lipopolysaccharide (LPS) treatment significantly. Also, STC2 pretreatment significantly decreased
TNF-α and
IL-1β expression induced by LPS treatment. These observations demonstrated that STC2 exerts neuroprotective actions against excitotoxic insults through the inhibition of microglial activation. |
| doi_str_mv | 10.1016/j.peptides.2010.08.002 |
| format | Article |
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Stanniocalcin 2 (STC2), the paralog of STC1, has been shown to act as a novel target of the mammalian unfolded protein response. We investigated the potential neuroprotective actions of STC2 against kainic acid toxicity in the hippocampus of ICR mice. STC2-treated mice experienced less neuronal cell loss in the CA3 area of the hippocampus. Also, microglial activation and heme oxygenase 1 expression were attenuated in the hippocampus of STC2-treated mice. To confirm whether STC2 regulates microglial activation directly, nitric oxide levels were measured in BV2 cells cultured with and without 10
nM STC2. STC2 decreased the level of nitric oxide induced by lipopolysaccharide (LPS) treatment significantly. Also, STC2 pretreatment significantly decreased
TNF-α and
IL-1β expression induced by LPS treatment. These observations demonstrated that STC2 exerts neuroprotective actions against excitotoxic insults through the inhibition of microglial activation.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/j.peptides.2010.08.002</identifier><identifier>PMID: 20713105</identifier><identifier>CODEN: PPTDD5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Activation ; Animals ; Attenuation ; Biological and medical sciences ; BV2 cells ; Cell Death - drug effects ; Degeneration ; Fundamental and applied biological sciences. Psychology ; Glycoproteins - pharmacology ; Heme Oxygenase-1 - biosynthesis ; Hippocampus ; Hippocampus - metabolism ; Inhibition ; Interleukin-1beta - biosynthesis ; Kainic acid ; Kainic Acid - antagonists & inhibitors ; Lipopolysaccharides ; Male ; Mice ; Mice, Inbred ICR ; Microglia - drug effects ; Microglia - metabolism ; Microglial activation ; Neuroprotective Agents - pharmacology ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - biosynthesis ; Proteins ; Stanniocalcin 2 ; Toxicity ; Tumor Necrosis Factor-alpha - biosynthesis ; Vertebrates: endocrinology</subject><ispartof>Peptides (New York, N.Y. : 1980), 2010-11, Vol.31 (11), p.2094-2099</ispartof><rights>2010 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-8f1e9f11a68e071d1fdf3d71d68050142a5fce0cf7dd2e6479658966528e07983</citedby><cites>FETCH-LOGICAL-c462t-8f1e9f11a68e071d1fdf3d71d68050142a5fce0cf7dd2e6479658966528e07983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.peptides.2010.08.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23383516$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20713105$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Byun, Jong-Seon</creatorcontrib><creatorcontrib>Lee, Jae-Won</creatorcontrib><creatorcontrib>Kim, Su Young</creatorcontrib><creatorcontrib>Kwon, Kwang Jun</creatorcontrib><creatorcontrib>Sohn, Jong-Hee</creatorcontrib><creatorcontrib>Lee, Kyunyoung</creatorcontrib><creatorcontrib>Oh, Dahlkyun</creatorcontrib><creatorcontrib>Kim, Sung-Soo</creatorcontrib><creatorcontrib>Chun, Wanjoo</creatorcontrib><creatorcontrib>Lee, Hee Jae</creatorcontrib><title>Neuroprotective effects of stanniocalcin 2 following kainic acid-induced hippocampal degeneration in ICR mice</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>▶ STC2 attenuates KA-induced neuronal death. ▶ STC2 attenuates KA-induced microglial activation. ▶ STC2 attenuates KA-induced HO-1 expression in the glial cells. ▶ STC2 inhibits expression levels of NO, TNF-α, and IL-1β in LPS-stimulated BV2 cells.
Stanniocalcin 2 (STC2), the paralog of STC1, has been shown to act as a novel target of the mammalian unfolded protein response. We investigated the potential neuroprotective actions of STC2 against kainic acid toxicity in the hippocampus of ICR mice. STC2-treated mice experienced less neuronal cell loss in the CA3 area of the hippocampus. Also, microglial activation and heme oxygenase 1 expression were attenuated in the hippocampus of STC2-treated mice. To confirm whether STC2 regulates microglial activation directly, nitric oxide levels were measured in BV2 cells cultured with and without 10
nM STC2. STC2 decreased the level of nitric oxide induced by lipopolysaccharide (LPS) treatment significantly. Also, STC2 pretreatment significantly decreased
TNF-α and
IL-1β expression induced by LPS treatment. These observations demonstrated that STC2 exerts neuroprotective actions against excitotoxic insults through the inhibition of microglial activation.</description><subject>Activation</subject><subject>Animals</subject><subject>Attenuation</subject><subject>Biological and medical sciences</subject><subject>BV2 cells</subject><subject>Cell Death - drug effects</subject><subject>Degeneration</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycoproteins - pharmacology</subject><subject>Heme Oxygenase-1 - biosynthesis</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Inhibition</subject><subject>Interleukin-1beta - biosynthesis</subject><subject>Kainic acid</subject><subject>Kainic Acid - antagonists & inhibitors</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Microglial activation</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - biosynthesis</subject><subject>Proteins</subject><subject>Stanniocalcin 2</subject><subject>Toxicity</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Vertebrates: endocrinology</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGOFCEQhonRuOPqK2y4GL30SNHdNNw0k9XdZKOJ0TNBKFbGbmihe41vL5OZXW96okK-H6rqI-QC2BYYiDf77YzzEhyWLWf1ksktY_wR2YAc2qYHoR6TDQMlGjVIOCPPStkzxrpOyafkjLMBWmD9hkwfcc1pzmlBu4Q7pOh9rQpNnpbFxBiSNaMNkXLq0zimXyHe0h8mxGCpscE1IbrVoqPfwzxXdprNSB3eYsRslpAirdnr3Wc6BYvPyRNvxoIvTuc5-fr-8svuqrn59OF69-6msZ3gSyM9oPIARkisnTrwzreuFkKynkHHTe8tMusH5ziKblCil0qInh94Jdtz8ur4bh3s54pl0VMoFsfRRExr0ZINLQPgUMnX_yRhEBxgANVXVBxRm1MpGb2ec5hM_q2B6YMUvdf3UvRBimZSVyk1eHH6Y_02oXuI3VuowMsTYErdts8m2lD-cm0r26q0cm-PHNbd3QXMutiAsW4_5CpNuxT-18sfhLauZA</recordid><startdate>20101101</startdate><enddate>20101101</enddate><creator>Byun, Jong-Seon</creator><creator>Lee, Jae-Won</creator><creator>Kim, Su Young</creator><creator>Kwon, Kwang Jun</creator><creator>Sohn, Jong-Hee</creator><creator>Lee, Kyunyoung</creator><creator>Oh, Dahlkyun</creator><creator>Kim, Sung-Soo</creator><creator>Chun, Wanjoo</creator><creator>Lee, Hee Jae</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7U5</scope><scope>8FD</scope><scope>L7M</scope><scope>7TK</scope></search><sort><creationdate>20101101</creationdate><title>Neuroprotective effects of stanniocalcin 2 following kainic acid-induced hippocampal degeneration in ICR mice</title><author>Byun, Jong-Seon ; Lee, Jae-Won ; Kim, Su Young ; Kwon, Kwang Jun ; Sohn, Jong-Hee ; Lee, Kyunyoung ; Oh, Dahlkyun ; Kim, Sung-Soo ; Chun, Wanjoo ; Lee, Hee Jae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-8f1e9f11a68e071d1fdf3d71d68050142a5fce0cf7dd2e6479658966528e07983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Activation</topic><topic>Animals</topic><topic>Attenuation</topic><topic>Biological and medical sciences</topic><topic>BV2 cells</topic><topic>Cell Death - drug effects</topic><topic>Degeneration</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycoproteins - pharmacology</topic><topic>Heme Oxygenase-1 - biosynthesis</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Inhibition</topic><topic>Interleukin-1beta - biosynthesis</topic><topic>Kainic acid</topic><topic>Kainic Acid - antagonists & inhibitors</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Microglial activation</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - biosynthesis</topic><topic>Proteins</topic><topic>Stanniocalcin 2</topic><topic>Toxicity</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Byun, Jong-Seon</creatorcontrib><creatorcontrib>Lee, Jae-Won</creatorcontrib><creatorcontrib>Kim, Su Young</creatorcontrib><creatorcontrib>Kwon, Kwang Jun</creatorcontrib><creatorcontrib>Sohn, Jong-Hee</creatorcontrib><creatorcontrib>Lee, Kyunyoung</creatorcontrib><creatorcontrib>Oh, Dahlkyun</creatorcontrib><creatorcontrib>Kim, Sung-Soo</creatorcontrib><creatorcontrib>Chun, Wanjoo</creatorcontrib><creatorcontrib>Lee, Hee Jae</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Neurosciences Abstracts</collection><jtitle>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Byun, Jong-Seon</au><au>Lee, Jae-Won</au><au>Kim, Su Young</au><au>Kwon, Kwang Jun</au><au>Sohn, Jong-Hee</au><au>Lee, Kyunyoung</au><au>Oh, Dahlkyun</au><au>Kim, Sung-Soo</au><au>Chun, Wanjoo</au><au>Lee, Hee Jae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective effects of stanniocalcin 2 following kainic acid-induced hippocampal degeneration in ICR mice</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>31</volume><issue>11</issue><spage>2094</spage><epage>2099</epage><pages>2094-2099</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><coden>PPTDD5</coden><abstract>▶ STC2 attenuates KA-induced neuronal death. ▶ STC2 attenuates KA-induced microglial activation. ▶ STC2 attenuates KA-induced HO-1 expression in the glial cells. ▶ STC2 inhibits expression levels of NO, TNF-α, and IL-1β in LPS-stimulated BV2 cells.
Stanniocalcin 2 (STC2), the paralog of STC1, has been shown to act as a novel target of the mammalian unfolded protein response. We investigated the potential neuroprotective actions of STC2 against kainic acid toxicity in the hippocampus of ICR mice. STC2-treated mice experienced less neuronal cell loss in the CA3 area of the hippocampus. Also, microglial activation and heme oxygenase 1 expression were attenuated in the hippocampus of STC2-treated mice. To confirm whether STC2 regulates microglial activation directly, nitric oxide levels were measured in BV2 cells cultured with and without 10
nM STC2. STC2 decreased the level of nitric oxide induced by lipopolysaccharide (LPS) treatment significantly. Also, STC2 pretreatment significantly decreased
TNF-α and
IL-1β expression induced by LPS treatment. These observations demonstrated that STC2 exerts neuroprotective actions against excitotoxic insults through the inhibition of microglial activation.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>20713105</pmid><doi>10.1016/j.peptides.2010.08.002</doi><tpages>6</tpages></addata></record> |
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| subjects | Activation Animals Attenuation Biological and medical sciences BV2 cells Cell Death - drug effects Degeneration Fundamental and applied biological sciences. Psychology Glycoproteins - pharmacology Heme Oxygenase-1 - biosynthesis Hippocampus Hippocampus - metabolism Inhibition Interleukin-1beta - biosynthesis Kainic acid Kainic Acid - antagonists & inhibitors Lipopolysaccharides Male Mice Mice, Inbred ICR Microglia - drug effects Microglia - metabolism Microglial activation Neuroprotective Agents - pharmacology Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type II - biosynthesis Proteins Stanniocalcin 2 Toxicity Tumor Necrosis Factor-alpha - biosynthesis Vertebrates: endocrinology |
| title | Neuroprotective effects of stanniocalcin 2 following kainic acid-induced hippocampal degeneration in ICR mice |
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