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Electromagnetic pulse activated brain microglia via the p38 MAPK pathway
•EMP exposure could activate microglia and affect its secretion function.•p38 pathway was involved. Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate mic...
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| Published in: | Neurotoxicology (Park Forest South) 2016-01, Vol.52, p.144-149 |
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| container_title | Neurotoxicology (Park Forest South) |
| container_volume | 52 |
| creator | Yang, Long-Long Zhou, Yan Tian, Wei-Dong Li, Hai-Juan Kang-Chu-Li Miao, Xia An, Guang-Zhou Wang, Xiao-Wu Guo, Guo-Zhen Ding, Gui-Rong |
| description | •EMP exposure could activate microglia and affect its secretion function.•p38 pathway was involved.
Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1β, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p |
| doi_str_mv | 10.1016/j.neuro.2015.12.008 |
| format | article |
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Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1β, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p<0.05) and recovered to the sham group level at 24h after EMP exposure. Levels of NO, TNF-α and IL-10 also changed significantly in vivo and in vitro after EMP exposure. The protein level of p38 and phosphorylated p38 increased significantly after EMP exposure (p<0.05) and recovered to sham levels at 12 and 24h, respectively. Protein and phosphorylated protein levels of ERK and JNK did not change. SB203580 (p38 inhibitor) partly prevented the change in NO, IL-10, IL-1β, TNF-α levels induced by EMP exposure. Taken together, these results suggested that EMP exposure (200kV/m, 200 pulses) could activate microglia in rat brain and affect its secretory function both in vivo and in vitro, and the p38 pathway is involved in this process.</description><identifier>ISSN: 0161-813X</identifier><identifier>EISSN: 1872-9711</identifier><identifier>DOI: 10.1016/j.neuro.2015.12.008</identifier><identifier>PMID: 26688329</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Brain ; Cerebral Cortex - cytology ; Electromagnetic Fields - adverse effects ; Electromagnetic pulse ; Imidazoles - pharmacology ; Interleukin-10 - metabolism ; Interleukin-1beta - metabolism ; Male ; MAP Kinase Signaling System - drug effects ; MAPK pathway ; Microglia ; Microglia - drug effects ; Microglia - metabolism ; Nitric Oxide - metabolism ; p38 Mitogen-Activated Protein Kinases - metabolism ; Primary Cell Culture ; Pyridines - pharmacology ; Rats ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Neurotoxicology (Park Forest South), 2016-01, Vol.52, p.144-149</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-dcd57b98310cae5b7ed49b7bf5436c92cdac09ae3c8b496be412bd83a8dc06d63</citedby><cites>FETCH-LOGICAL-c392t-dcd57b98310cae5b7ed49b7bf5436c92cdac09ae3c8b496be412bd83a8dc06d63</cites><orcidid>0000-0003-3641-6545</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26688329$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Long-Long</creatorcontrib><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Tian, Wei-Dong</creatorcontrib><creatorcontrib>Li, Hai-Juan</creatorcontrib><creatorcontrib>Kang-Chu-Li</creatorcontrib><creatorcontrib>Miao, Xia</creatorcontrib><creatorcontrib>An, Guang-Zhou</creatorcontrib><creatorcontrib>Wang, Xiao-Wu</creatorcontrib><creatorcontrib>Guo, Guo-Zhen</creatorcontrib><creatorcontrib>Ding, Gui-Rong</creatorcontrib><title>Electromagnetic pulse activated brain microglia via the p38 MAPK pathway</title><title>Neurotoxicology (Park Forest South)</title><addtitle>Neurotoxicology</addtitle><description>•EMP exposure could activate microglia and affect its secretion function.•p38 pathway was involved.
Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1β, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p<0.05) and recovered to the sham group level at 24h after EMP exposure. Levels of NO, TNF-α and IL-10 also changed significantly in vivo and in vitro after EMP exposure. The protein level of p38 and phosphorylated p38 increased significantly after EMP exposure (p<0.05) and recovered to sham levels at 12 and 24h, respectively. Protein and phosphorylated protein levels of ERK and JNK did not change. SB203580 (p38 inhibitor) partly prevented the change in NO, IL-10, IL-1β, TNF-α levels induced by EMP exposure. Taken together, these results suggested that EMP exposure (200kV/m, 200 pulses) could activate microglia in rat brain and affect its secretory function both in vivo and in vitro, and the p38 pathway is involved in this process.</description><subject>Animals</subject><subject>Brain</subject><subject>Cerebral Cortex - cytology</subject><subject>Electromagnetic Fields - adverse effects</subject><subject>Electromagnetic pulse</subject><subject>Imidazoles - pharmacology</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAPK pathway</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Primary Cell Culture</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0161-813X</issn><issn>1872-9711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkDlPJDEQRq0VaBnY_QVIqEOSbnx0-wgIEOISIAhA2szyUQMe9YXdPYh_j9kBwtUGpUreV5_qIbRPcEUw4Uerqoc5DhXFpKkIrTCWP9CCSEFLJQjZQotMkVIS9mcH7aa0whkUXP1EO5RzKRlVC3R51oKb4tCZpx6m4IpxbhMUxk1hbSbwhY0m9EUXXBye2mCKdZ7pGYqRyeL25P66GM30_GrefqHtpcnR3597Dz2enz2cXpY3dxdXpyc3pWOKTqV3vhFWSUawM9BYAb5WVthlUzPuFHXeOKwMMCdtrbiFmlDrJTPSO8w9Z3vocHN3jMPLDGnSXUgO2tb0MMxJE8FlI7Ai4n_QhjHKZZ1RtkHzmylFWOoxhs7EN02w_rCtV_qvbf1hWxOqs-2cOvgsmG0H_jvzpTcDxxsAspF1gKiTC9A78CFm7doP4Z8F782Wka8</recordid><startdate>201601</startdate><enddate>201601</enddate><creator>Yang, Long-Long</creator><creator>Zhou, Yan</creator><creator>Tian, Wei-Dong</creator><creator>Li, Hai-Juan</creator><creator>Kang-Chu-Li</creator><creator>Miao, Xia</creator><creator>An, Guang-Zhou</creator><creator>Wang, Xiao-Wu</creator><creator>Guo, Guo-Zhen</creator><creator>Ding, Gui-Rong</creator><general>Elsevier 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>7X8</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><orcidid>https://orcid.org/0000-0003-3641-6545</orcidid></search><sort><creationdate>201601</creationdate><title>Electromagnetic pulse activated brain microglia via the p38 MAPK pathway</title><author>Yang, Long-Long ; Zhou, Yan ; Tian, Wei-Dong ; Li, Hai-Juan ; Kang-Chu-Li ; Miao, Xia ; An, Guang-Zhou ; Wang, Xiao-Wu ; Guo, Guo-Zhen ; Ding, Gui-Rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-dcd57b98310cae5b7ed49b7bf5436c92cdac09ae3c8b496be412bd83a8dc06d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Brain</topic><topic>Cerebral Cortex - cytology</topic><topic>Electromagnetic Fields - adverse effects</topic><topic>Electromagnetic pulse</topic><topic>Imidazoles - pharmacology</topic><topic>Interleukin-10 - metabolism</topic><topic>Interleukin-1beta - metabolism</topic><topic>Male</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAPK pathway</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Primary Cell Culture</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Long-Long</creatorcontrib><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Tian, Wei-Dong</creatorcontrib><creatorcontrib>Li, Hai-Juan</creatorcontrib><creatorcontrib>Kang-Chu-Li</creatorcontrib><creatorcontrib>Miao, Xia</creatorcontrib><creatorcontrib>An, Guang-Zhou</creatorcontrib><creatorcontrib>Wang, Xiao-Wu</creatorcontrib><creatorcontrib>Guo, Guo-Zhen</creatorcontrib><creatorcontrib>Ding, Gui-Rong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicology (Park Forest South)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Long-Long</au><au>Zhou, Yan</au><au>Tian, Wei-Dong</au><au>Li, Hai-Juan</au><au>Kang-Chu-Li</au><au>Miao, Xia</au><au>An, Guang-Zhou</au><au>Wang, Xiao-Wu</au><au>Guo, Guo-Zhen</au><au>Ding, Gui-Rong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electromagnetic pulse activated brain microglia via the p38 MAPK pathway</atitle><jtitle>Neurotoxicology (Park Forest South)</jtitle><addtitle>Neurotoxicology</addtitle><date>2016-01</date><risdate>2016</risdate><volume>52</volume><spage>144</spage><epage>149</epage><pages>144-149</pages><issn>0161-813X</issn><eissn>1872-9711</eissn><abstract>•EMP exposure could activate microglia and affect its secretion function.•p38 pathway was involved.
Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1β, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p<0.05) and recovered to the sham group level at 24h after EMP exposure. Levels of NO, TNF-α and IL-10 also changed significantly in vivo and in vitro after EMP exposure. The protein level of p38 and phosphorylated p38 increased significantly after EMP exposure (p<0.05) and recovered to sham levels at 12 and 24h, respectively. Protein and phosphorylated protein levels of ERK and JNK did not change. SB203580 (p38 inhibitor) partly prevented the change in NO, IL-10, IL-1β, TNF-α levels induced by EMP exposure. Taken together, these results suggested that EMP exposure (200kV/m, 200 pulses) could activate microglia in rat brain and affect its secretory function both in vivo and in vitro, and the p38 pathway is involved in this process.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26688329</pmid><doi>10.1016/j.neuro.2015.12.008</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0003-3641-6545</orcidid></addata></record> |
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| subjects | Animals Brain Cerebral Cortex - cytology Electromagnetic Fields - adverse effects Electromagnetic pulse Imidazoles - pharmacology Interleukin-10 - metabolism Interleukin-1beta - metabolism Male MAP Kinase Signaling System - drug effects MAPK pathway Microglia Microglia - drug effects Microglia - metabolism Nitric Oxide - metabolism p38 Mitogen-Activated Protein Kinases - metabolism Primary Cell Culture Pyridines - pharmacology Rats Tumor Necrosis Factor-alpha - metabolism |
| title | Electromagnetic pulse activated brain microglia via the p38 MAPK pathway |
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