Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway
Previously, we found that exposure to a 50‐Hz magnetic field (MF) could induce human amniotic epithelial (FL) cell proliferation and sphingosine kinase 1 (SK1) activation, but the mechanism was not clearly understood. In the present study, the possible signaling pathways which were involved in SK1 a...
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Veröffentlicht in: | Bioelectromagnetics 2019-04, Vol.40 (3), p.180-187 |
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description | Previously, we found that exposure to a 50‐Hz magnetic field (MF) could induce human amniotic epithelial (FL) cell proliferation and sphingosine kinase 1 (SK1) activation, but the mechanism was not clearly understood. In the present study, the possible signaling pathways which were involved in SK1 activation induced by 50‐Hz MF exposure were investigated. Results showed that MF exposure increased intracellular Ca2+ which was dependent on the L‐type calcium channel, and induced Ca2+‐dependent phosphorylation of extracellular regulated protein kinase (ERK), SK1, and protein kinase C α (PKCα). Also, treatment with U0126, an inhibitor of ERK, could block MF‐induced SK1 phosphorylation, but had no effect on PKCα phosphorylation. Also, the inhibitor of PKCα, Gö6976, had no effect on MF‐induced SK1 activation in FL cells. In addition, the activation of ERK and PKCα could be abolished by SKI II, the inhibitor of SK1. In conclusion, the intracellular Ca2+ mediated the 50‐Hz MF‐induced SK1 activation which enhanced PKCα phosphorylation, and there might be a feedback mechanism between SK1 and ERK activation in responding to MF exposure in FL cells. Bioelectromagnetics. 9999:XX–XX, 2019. © 2019 Bioelectromagnetics Society. |
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In the present study, the possible signaling pathways which were involved in SK1 activation induced by 50‐Hz MF exposure were investigated. Results showed that MF exposure increased intracellular Ca2+ which was dependent on the L‐type calcium channel, and induced Ca2+‐dependent phosphorylation of extracellular regulated protein kinase (ERK), SK1, and protein kinase C α (PKCα). Also, treatment with U0126, an inhibitor of ERK, could block MF‐induced SK1 phosphorylation, but had no effect on PKCα phosphorylation. Also, the inhibitor of PKCα, Gö6976, had no effect on MF‐induced SK1 activation in FL cells. In addition, the activation of ERK and PKCα could be abolished by SKI II, the inhibitor of SK1. In conclusion, the intracellular Ca2+ mediated the 50‐Hz MF‐induced SK1 activation which enhanced PKCα phosphorylation, and there might be a feedback mechanism between SK1 and ERK activation in responding to MF exposure in FL cells. Bioelectromagnetics. 9999:XX–XX, 2019. © 2019 Bioelectromagnetics Society.</description><identifier>ISSN: 0197-8462</identifier><identifier>EISSN: 1521-186X</identifier><identifier>DOI: 10.1002/bem.22181</identifier><identifier>PMID: 30920672</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>50‐Hz magnetic field (MF) ; Activation ; Calcium ; Calcium (extracellular) ; Calcium (intracellular) ; Calcium ions ; Cell proliferation ; Exposure ; extracellular regulated protein kinase (ERK) ; Extracellular signal-regulated kinase ; Inhibitors ; Intracellular ; intracellular Ca2 ; Kinases ; Magnetic fields ; Phosphorylation ; Protein kinase C ; protein kinase Cα (PKCα) ; Proteins ; Signal transduction ; Signaling ; Sphingosine kinase ; Sphingosine kinase 1 (SK1)</subject><ispartof>Bioelectromagnetics, 2019-04, Vol.40 (3), p.180-187</ispartof><rights>2019 Bioelectromagnetics Society</rights><rights>2019 Bioelectromagnetics Society.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2831-1af499c70f2653a7586d29a5e75039c9054bf6ba56c32951677bf4fa96a235933</citedby><cites>FETCH-LOGICAL-c2831-1af499c70f2653a7586d29a5e75039c9054bf6ba56c32951677bf4fa96a235933</cites><orcidid>0000-0003-4336-6494</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fbem.22181$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fbem.22181$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30920672$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Xiaobo</creatorcontrib><creatorcontrib>Ye, Anfang</creatorcontrib><creatorcontrib>Chen, Liangjing</creatorcontrib><creatorcontrib>Xia, Yongpeng</creatorcontrib><creatorcontrib>Jiang, Wei</creatorcontrib><creatorcontrib>Sun, Wenjun</creatorcontrib><title>Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway</title><title>Bioelectromagnetics</title><addtitle>Bioelectromagnetics</addtitle><description>Previously, we found that exposure to a 50‐Hz magnetic field (MF) could induce human amniotic epithelial (FL) cell proliferation and sphingosine kinase 1 (SK1) activation, but the mechanism was not clearly understood. In the present study, the possible signaling pathways which were involved in SK1 activation induced by 50‐Hz MF exposure were investigated. Results showed that MF exposure increased intracellular Ca2+ which was dependent on the L‐type calcium channel, and induced Ca2+‐dependent phosphorylation of extracellular regulated protein kinase (ERK), SK1, and protein kinase C α (PKCα). Also, treatment with U0126, an inhibitor of ERK, could block MF‐induced SK1 phosphorylation, but had no effect on PKCα phosphorylation. Also, the inhibitor of PKCα, Gö6976, had no effect on MF‐induced SK1 activation in FL cells. In addition, the activation of ERK and PKCα could be abolished by SKI II, the inhibitor of SK1. In conclusion, the intracellular Ca2+ mediated the 50‐Hz MF‐induced SK1 activation which enhanced PKCα phosphorylation, and there might be a feedback mechanism between SK1 and ERK activation in responding to MF exposure in FL cells. Bioelectromagnetics. 9999:XX–XX, 2019. © 2019 Bioelectromagnetics Society.</description><subject>50‐Hz magnetic field (MF)</subject><subject>Activation</subject><subject>Calcium</subject><subject>Calcium (extracellular)</subject><subject>Calcium (intracellular)</subject><subject>Calcium ions</subject><subject>Cell proliferation</subject><subject>Exposure</subject><subject>extracellular regulated protein kinase (ERK)</subject><subject>Extracellular signal-regulated kinase</subject><subject>Inhibitors</subject><subject>Intracellular</subject><subject>intracellular Ca2</subject><subject>Kinases</subject><subject>Magnetic fields</subject><subject>Phosphorylation</subject><subject>Protein kinase C</subject><subject>protein kinase Cα (PKCα)</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Sphingosine kinase</subject><subject>Sphingosine kinase 1 (SK1)</subject><issn>0197-8462</issn><issn>1521-186X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp10c1O3DAUBWCrKirTgUVfoLLUDSwG_BM79rKMoIMEYgMSu-jGsQfTxJ7GyaBhxSP0GfskGIZ2UYmVpavPR_Y9CH2h5IgSwo5r2x0xRhX9gCZUMDqjSt5-RBNCdTlThWS76HNK94QQpQj_hHY50YzIkk1QPA_r2K5tZ8OAo8MGWuPHDvuABfnz9HvxiDtYBjt4g523bZNnPjSjsQ0GM_g1DD6Gl5tpdefDMiYfLP7pAySLKU5-GaDNc7yC4e4BNntox0Gb7P7bOUU3Z6fX88Xs4urH-fz7xcwwxfMHwBVam5I4JgWHUijZMA3CloJwbTQRRe1kDUIazrSgsixrVzjQEhgXmvMpOtjmrvr4a7RpqDqfjG1bCDaOqWJUa6qULIpMv_1H7-PY52e_KiUKRbTI6nCrTB9T6q2rVr3voN9UlFQvLVS5heq1hWy_viWOdWebf_Lv2jM43oIH39rN-0nVyenlNvIZKhSR0Q</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Yang, Xiaobo</creator><creator>Ye, Anfang</creator><creator>Chen, Liangjing</creator><creator>Xia, Yongpeng</creator><creator>Jiang, Wei</creator><creator>Sun, Wenjun</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-4336-6494</orcidid></search><sort><creationdate>201904</creationdate><title>Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway</title><author>Yang, Xiaobo ; Ye, Anfang ; Chen, Liangjing ; Xia, Yongpeng ; Jiang, Wei ; Sun, Wenjun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2831-1af499c70f2653a7586d29a5e75039c9054bf6ba56c32951677bf4fa96a235933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>50‐Hz magnetic field (MF)</topic><topic>Activation</topic><topic>Calcium</topic><topic>Calcium (extracellular)</topic><topic>Calcium (intracellular)</topic><topic>Calcium ions</topic><topic>Cell proliferation</topic><topic>Exposure</topic><topic>extracellular regulated protein kinase (ERK)</topic><topic>Extracellular signal-regulated kinase</topic><topic>Inhibitors</topic><topic>Intracellular</topic><topic>intracellular Ca2</topic><topic>Kinases</topic><topic>Magnetic fields</topic><topic>Phosphorylation</topic><topic>Protein kinase C</topic><topic>protein kinase Cα (PKCα)</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Sphingosine kinase</topic><topic>Sphingosine kinase 1 (SK1)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Xiaobo</creatorcontrib><creatorcontrib>Ye, Anfang</creatorcontrib><creatorcontrib>Chen, Liangjing</creatorcontrib><creatorcontrib>Xia, Yongpeng</creatorcontrib><creatorcontrib>Jiang, Wei</creatorcontrib><creatorcontrib>Sun, Wenjun</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Bioelectromagnetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Xiaobo</au><au>Ye, Anfang</au><au>Chen, Liangjing</au><au>Xia, Yongpeng</au><au>Jiang, Wei</au><au>Sun, Wenjun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway</atitle><jtitle>Bioelectromagnetics</jtitle><addtitle>Bioelectromagnetics</addtitle><date>2019-04</date><risdate>2019</risdate><volume>40</volume><issue>3</issue><spage>180</spage><epage>187</epage><pages>180-187</pages><issn>0197-8462</issn><eissn>1521-186X</eissn><abstract>Previously, we found that exposure to a 50‐Hz magnetic field (MF) could induce human amniotic epithelial (FL) cell proliferation and sphingosine kinase 1 (SK1) activation, but the mechanism was not clearly understood. In the present study, the possible signaling pathways which were involved in SK1 activation induced by 50‐Hz MF exposure were investigated. Results showed that MF exposure increased intracellular Ca2+ which was dependent on the L‐type calcium channel, and induced Ca2+‐dependent phosphorylation of extracellular regulated protein kinase (ERK), SK1, and protein kinase C α (PKCα). Also, treatment with U0126, an inhibitor of ERK, could block MF‐induced SK1 phosphorylation, but had no effect on PKCα phosphorylation. Also, the inhibitor of PKCα, Gö6976, had no effect on MF‐induced SK1 activation in FL cells. In addition, the activation of ERK and PKCα could be abolished by SKI II, the inhibitor of SK1. In conclusion, the intracellular Ca2+ mediated the 50‐Hz MF‐induced SK1 activation which enhanced PKCα phosphorylation, and there might be a feedback mechanism between SK1 and ERK activation in responding to MF exposure in FL cells. Bioelectromagnetics. 9999:XX–XX, 2019. © 2019 Bioelectromagnetics Society.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30920672</pmid><doi>10.1002/bem.22181</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-4336-6494</orcidid></addata></record> |
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subjects | 50‐Hz magnetic field (MF) Activation Calcium Calcium (extracellular) Calcium (intracellular) Calcium ions Cell proliferation Exposure extracellular regulated protein kinase (ERK) Extracellular signal-regulated kinase Inhibitors Intracellular intracellular Ca2 Kinases Magnetic fields Phosphorylation Protein kinase C protein kinase Cα (PKCα) Proteins Signal transduction Signaling Sphingosine kinase Sphingosine kinase 1 (SK1) |
title | Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway |
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