Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats
The aim of this study was to investigate the pathogenesis of autophagy and apoptosis mediated by Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signal pathway after the onset of acute spinal cord injury (ASCI). A total of 45 Sprague-Dawley adult rats of either sex wer...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2017-08, Vol.14 (2), p.1589-1593 |
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| description | The aim of this study was to investigate the pathogenesis of autophagy and apoptosis mediated by Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signal pathway after the onset of acute spinal cord injury (ASCI). A total of 45 Sprague-Dawley adult rats of either sex were selected for this study. The age of rats ranged from 8 to 10 weeks, and the average weight was 245 g. These rats were randomly divided into three groups, i.e. sham-operated group, model group, and the AG-490 intervention group (AG-490 is an inhibitor of JAK2). Each group contained 15 rats. Models were prepared using the modified Allen method. Five rats in each group were sacrificed at 6, 12 and 24 h, respectively, and the expression levels of p-JAK2 and p-STAT3 were detected in spinal cord tissue via western blot analysis. The levels of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected via ELISA, positive expression of light chain 3 (LC3)-II of microtubule-associated protein 1 via immunofluorescence labeling method, and mRNA expression levels of caspase-3 and Bax/Bcl-2 via RT-PCR. In the model group, the expression levels of p-JAK2, p-STAT3, IL-6, TNF-α and LC3-II, and the mRNA expression levels of caspase-3 and Bax/Bcl-2 at all time-points were significantly higher than those in the AG-490 intervention group, and the levels in the sham-operated group were the lowest (p |
| doi_str_mv | 10.3892/etm.2017.4674 |
| format | Article |
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A total of 45 Sprague-Dawley adult rats of either sex were selected for this study. The age of rats ranged from 8 to 10 weeks, and the average weight was 245 g. These rats were randomly divided into three groups, i.e. sham-operated group, model group, and the AG-490 intervention group (AG-490 is an inhibitor of JAK2). Each group contained 15 rats. Models were prepared using the modified Allen method. Five rats in each group were sacrificed at 6, 12 and 24 h, respectively, and the expression levels of p-JAK2 and p-STAT3 were detected in spinal cord tissue via western blot analysis. The levels of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected via ELISA, positive expression of light chain 3 (LC3)-II of microtubule-associated protein 1 via immunofluorescence labeling method, and mRNA expression levels of caspase-3 and Bax/Bcl-2 via RT-PCR. In the model group, the expression levels of p-JAK2, p-STAT3, IL-6, TNF-α and LC3-II, and the mRNA expression levels of caspase-3 and Bax/Bcl-2 at all time-points were significantly higher than those in the AG-490 intervention group, and the levels in the sham-operated group were the lowest (p<0.05). In the model group, peak levels of p-JAK2 and p-STAT3 were attained at 12 h, but a decline was seen at 24 h; while increasing trend was seen in other indicators. In conclusion, JAK2/STAT3 signal pathway can mediate the activity of autophagy and apoptosis in an early stage after the onset of ASCI of rat.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2017.4674</identifier><identifier>PMID: 28781630</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>acute spinal cord injury ; Apoptosis ; Autophagy ; Care and treatment ; Catheters ; Cell growth ; Cytokines ; Interleukins ; JAK2/STAT3 signal pathway ; Kinases ; Messenger RNA ; Proteins ; Rodents ; Signal transduction ; Spinal cord injuries ; Tumor necrosis factor-TNF</subject><ispartof>Experimental and therapeutic medicine, 2017-08, Vol.14 (2), p.1589-1593</ispartof><rights>Copyright: © Xia et al.</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Xia et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-89e9e7d9f28c4a2faf66af4f23099101804158c87a8e15d0664a31b1c7c368953</citedby><cites>FETCH-LOGICAL-c512t-89e9e7d9f28c4a2faf66af4f23099101804158c87a8e15d0664a31b1c7c368953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526089/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526089/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28781630$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xia, Yongzhi</creatorcontrib><creatorcontrib>Xia, Haijian</creatorcontrib><creatorcontrib>Chen, Dan</creatorcontrib><creatorcontrib>Liao, Zhengbu</creatorcontrib><creatorcontrib>Yan, Yi</creatorcontrib><title>Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>The aim of this study was to investigate the pathogenesis of autophagy and apoptosis mediated by Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signal pathway after the onset of acute spinal cord injury (ASCI). A total of 45 Sprague-Dawley adult rats of either sex were selected for this study. The age of rats ranged from 8 to 10 weeks, and the average weight was 245 g. These rats were randomly divided into three groups, i.e. sham-operated group, model group, and the AG-490 intervention group (AG-490 is an inhibitor of JAK2). Each group contained 15 rats. Models were prepared using the modified Allen method. Five rats in each group were sacrificed at 6, 12 and 24 h, respectively, and the expression levels of p-JAK2 and p-STAT3 were detected in spinal cord tissue via western blot analysis. The levels of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected via ELISA, positive expression of light chain 3 (LC3)-II of microtubule-associated protein 1 via immunofluorescence labeling method, and mRNA expression levels of caspase-3 and Bax/Bcl-2 via RT-PCR. In the model group, the expression levels of p-JAK2, p-STAT3, IL-6, TNF-α and LC3-II, and the mRNA expression levels of caspase-3 and Bax/Bcl-2 at all time-points were significantly higher than those in the AG-490 intervention group, and the levels in the sham-operated group were the lowest (p<0.05). In the model group, peak levels of p-JAK2 and p-STAT3 were attained at 12 h, but a decline was seen at 24 h; while increasing trend was seen in other indicators. In conclusion, JAK2/STAT3 signal pathway can mediate the activity of autophagy and apoptosis in an early stage after the onset of ASCI of rat.</description><subject>acute spinal cord injury</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Care and treatment</subject><subject>Catheters</subject><subject>Cell growth</subject><subject>Cytokines</subject><subject>Interleukins</subject><subject>JAK2/STAT3 signal pathway</subject><subject>Kinases</subject><subject>Messenger RNA</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Spinal cord injuries</subject><subject>Tumor necrosis factor-TNF</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptks-P1CAUxxujcTfrHr0aEmOyl45AS4GLyWSz_tyNl_VM3lDoMGlLBaqZ_36pM46ukXeAPD7vCw--RfGS4FUlJH1r0rCimPBV3fD6SXFOuKQlwYQ9Pa6xFOSsuIxxh_NgDRGCPS_OqOCCNBU-L9yd0VsYXRwi8hbBnPy0hW6PYGwRTH5KPrqIBtM6SKZFmz36vP5CUXTdCL0bOzRB2v6EXGCTCShOLueR9qFFbtzNYb_IBkjxRfHMQh_N5XG-KL69v7m__ljefv3w6Xp9W2pGaCqFNNLwVloqdA3Ugm0asLWlFZYytyZwTZjQgoMwhLW4aWqoyIZorqtGSFZdFO8OutO8ydfWZkwBejUFN0DYKw9OPd4Z3VZ1_odijDZYyCxwdRQI_vtsYlKDi9r0PYzGz1ERSRvJhSAko6__QXd-DvkBFkrWktVc4D9UB71RbrQ-n6sXUbVmuR3Oeb1orf5D5WjN4LQfjXU5_6igPBTo4GMMxp56JFgt9lDZHmqxh1rskflXfz_Mif5thgy8OQBxyr_vWh9PzM39XYlz_BJ6AH56wOE</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Xia, Yongzhi</creator><creator>Xia, Haijian</creator><creator>Chen, Dan</creator><creator>Liao, Zhengbu</creator><creator>Yan, Yi</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170801</creationdate><title>Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats</title><author>Xia, Yongzhi ; Xia, Haijian ; Chen, Dan ; Liao, Zhengbu ; Yan, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-89e9e7d9f28c4a2faf66af4f23099101804158c87a8e15d0664a31b1c7c368953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>acute spinal cord injury</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Care and treatment</topic><topic>Catheters</topic><topic>Cell growth</topic><topic>Cytokines</topic><topic>Interleukins</topic><topic>JAK2/STAT3 signal pathway</topic><topic>Kinases</topic><topic>Messenger RNA</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Spinal cord injuries</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xia, Yongzhi</creatorcontrib><creatorcontrib>Xia, Haijian</creatorcontrib><creatorcontrib>Chen, Dan</creatorcontrib><creatorcontrib>Liao, Zhengbu</creatorcontrib><creatorcontrib>Yan, Yi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xia, Yongzhi</au><au>Xia, Haijian</au><au>Chen, Dan</au><au>Liao, Zhengbu</au><au>Yan, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>14</volume><issue>2</issue><spage>1589</spage><epage>1593</epage><pages>1589-1593</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>The aim of this study was to investigate the pathogenesis of autophagy and apoptosis mediated by Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signal pathway after the onset of acute spinal cord injury (ASCI). A total of 45 Sprague-Dawley adult rats of either sex were selected for this study. The age of rats ranged from 8 to 10 weeks, and the average weight was 245 g. These rats were randomly divided into three groups, i.e. sham-operated group, model group, and the AG-490 intervention group (AG-490 is an inhibitor of JAK2). Each group contained 15 rats. Models were prepared using the modified Allen method. Five rats in each group were sacrificed at 6, 12 and 24 h, respectively, and the expression levels of p-JAK2 and p-STAT3 were detected in spinal cord tissue via western blot analysis. The levels of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected via ELISA, positive expression of light chain 3 (LC3)-II of microtubule-associated protein 1 via immunofluorescence labeling method, and mRNA expression levels of caspase-3 and Bax/Bcl-2 via RT-PCR. In the model group, the expression levels of p-JAK2, p-STAT3, IL-6, TNF-α and LC3-II, and the mRNA expression levels of caspase-3 and Bax/Bcl-2 at all time-points were significantly higher than those in the AG-490 intervention group, and the levels in the sham-operated group were the lowest (p<0.05). In the model group, peak levels of p-JAK2 and p-STAT3 were attained at 12 h, but a decline was seen at 24 h; while increasing trend was seen in other indicators. In conclusion, JAK2/STAT3 signal pathway can mediate the activity of autophagy and apoptosis in an early stage after the onset of ASCI of rat.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28781630</pmid><doi>10.3892/etm.2017.4674</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | acute spinal cord injury Apoptosis Autophagy Care and treatment Catheters Cell growth Cytokines Interleukins JAK2/STAT3 signal pathway Kinases Messenger RNA Proteins Rodents Signal transduction Spinal cord injuries Tumor necrosis factor-TNF |
| title | Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats |
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