Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury
Previous studies have suggested that impairment secondary to mechanical injury is a major cause of irreversible damage to the spinal cord. Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The a...
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| Veröffentlicht in: | Molecular medicine reports 2015-06, Vol.11 (6), p.4262-4266 |
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| creator | ZHANG, XUESONG CHEN, CHAO MA, SHENGZHONG WANG, YAN ZHANG, XUELIAN SU, XIAOJING |
| description | Previous studies have suggested that impairment secondary to mechanical injury is a major cause of irreversible damage to the spinal cord. Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The aim of the present study was to evaluate how changes in the expression levels of the cellular chemokine, monocyte chemoattractant peptide-1 (MCP-1), and the chemotaxis of inflammatory cells (monocytes and macrophages) are involved in the process of SCI. RNA interference methods were used to study the mechanisms that protect residual neurons after SCI in an attempt to explore novel, early interventions for managing SCI. Our results suggested that inhibiting inflammation alleviates nerve cell injury caused by apoptosis and provides a potentially important approach for the future treatment of secondary SCI. |
| doi_str_mv | 10.3892/mmr.2015.3330 |
| format | Article |
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Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The aim of the present study was to evaluate how changes in the expression levels of the cellular chemokine, monocyte chemoattractant peptide-1 (MCP-1), and the chemotaxis of inflammatory cells (monocytes and macrophages) are involved in the process of SCI. RNA interference methods were used to study the mechanisms that protect residual neurons after SCI in an attempt to explore novel, early interventions for managing SCI. Our results suggested that inhibiting inflammation alleviates nerve cell injury caused by apoptosis and provides a potentially important approach for the future treatment of secondary SCI.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2015.3330</identifier><identifier>PMID: 25672988</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Cell injury ; Chemokine CCL2 - genetics ; Chemokines ; Chemotaxis ; Development and progression ; Gangrene ; Gene Expression Regulation ; Inflammation ; Inflammation - genetics ; Inflammation - pathology ; Macrophages ; Male ; monocyte chemoattractant peptide-1 ; Monocyte chemoattractant protein 1 ; Monocytes ; Neurons - metabolism ; Neurons - pathology ; Physiological aspects ; Proteins ; Rats ; RNA Interference ; RNA, Messenger - genetics ; RNA, Small Interfering - genetics ; RNA-mediated interference ; Rodents ; secondary spinal cord injury ; Spinal cord injuries ; Spinal Cord Injuries - genetics ; Spinal Cord Injuries - pathology ; Studies ; Surgery</subject><ispartof>Molecular medicine reports, 2015-06, Vol.11 (6), p.4262-4266</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-1cb12e33cde2c5cc4cdd77e69545d094404c8b410460b85598af6a75de0cc7c93</citedby><cites>FETCH-LOGICAL-c459t-1cb12e33cde2c5cc4cdd77e69545d094404c8b410460b85598af6a75de0cc7c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5555,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25672988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHANG, XUESONG</creatorcontrib><creatorcontrib>CHEN, CHAO</creatorcontrib><creatorcontrib>MA, SHENGZHONG</creatorcontrib><creatorcontrib>WANG, YAN</creatorcontrib><creatorcontrib>ZHANG, XUELIAN</creatorcontrib><creatorcontrib>SU, XIAOJING</creatorcontrib><title>Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Previous studies have suggested that impairment secondary to mechanical injury is a major cause of irreversible damage to the spinal cord. Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The aim of the present study was to evaluate how changes in the expression levels of the cellular chemokine, monocyte chemoattractant peptide-1 (MCP-1), and the chemotaxis of inflammatory cells (monocytes and macrophages) are involved in the process of SCI. RNA interference methods were used to study the mechanisms that protect residual neurons after SCI in an attempt to explore novel, early interventions for managing SCI. Our results suggested that inhibiting inflammation alleviates nerve cell injury caused by apoptosis and provides a potentially important approach for the future treatment of secondary SCI.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Cell injury</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>Development and progression</subject><subject>Gangrene</subject><subject>Gene Expression Regulation</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - pathology</subject><subject>Macrophages</subject><subject>Male</subject><subject>monocyte chemoattractant peptide-1</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Rats</subject><subject>RNA Interference</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA-mediated interference</subject><subject>Rodents</subject><subject>secondary spinal cord injury</subject><subject>Spinal cord injuries</subject><subject>Spinal Cord Injuries - genetics</subject><subject>Spinal Cord Injuries - pathology</subject><subject>Studies</subject><subject>Surgery</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc1r3DAQxU1paNK0x16LoYf24o2-bR1D6Ecg0EtCj0IejRsttuRK9mH_-8jsNqWlmoPE8Jun4b2qekfJjneaXU1T2jFC5Y5zTl5UF7TVtOGEiJenN9O6Pa9e57wnREkm9avqnEnVMt11F9WP2_Doe7_4GOo41FMMEQ4L1vCIU7TLkiwsNiz1jPPiHTa0dggJbcZcZ4QYnE2HOs8-2LGGmFztw35NhzfV2WDHjG9P92X18OXz_c235u7719ub67sGhNRLQ6GnDDkHhwwkgADn2haVlkI6ooUgArpeUCIU6TspdWcHZVvpkAC0oPll9emoO6f4a8W8mMlnwHG0AeOaDVVKlMM6UdAP_6D7uKayd6E0Z0K1HWF_qJ92ROPDEDcPNlFzLRhpO8r19u3uP1Qph5MvruDgS_-vgeY4ACnmnHAwc_JT8c5QYrYgTQnSbEGaLcjCvz8tu_YTumf6d3IF-HgE8myD8y7mZ6YoNZQ2RDWCKcafALpepOY</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>ZHANG, XUESONG</creator><creator>CHEN, CHAO</creator><creator>MA, SHENGZHONG</creator><creator>WANG, YAN</creator><creator>ZHANG, XUELIAN</creator><creator>SU, XIAOJING</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150601</creationdate><title>Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury</title><author>ZHANG, XUESONG ; CHEN, CHAO ; MA, SHENGZHONG ; WANG, YAN ; ZHANG, XUELIAN ; SU, XIAOJING</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-1cb12e33cde2c5cc4cdd77e69545d094404c8b410460b85598af6a75de0cc7c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Cell injury</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokines</topic><topic>Chemotaxis</topic><topic>Development and progression</topic><topic>Gangrene</topic><topic>Gene Expression Regulation</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - pathology</topic><topic>Macrophages</topic><topic>Male</topic><topic>monocyte chemoattractant peptide-1</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Rats</topic><topic>RNA Interference</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA-mediated interference</topic><topic>Rodents</topic><topic>secondary spinal cord injury</topic><topic>Spinal cord injuries</topic><topic>Spinal Cord Injuries - genetics</topic><topic>Spinal Cord Injuries - pathology</topic><topic>Studies</topic><topic>Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHANG, XUESONG</creatorcontrib><creatorcontrib>CHEN, CHAO</creatorcontrib><creatorcontrib>MA, SHENGZHONG</creatorcontrib><creatorcontrib>WANG, YAN</creatorcontrib><creatorcontrib>ZHANG, XUELIAN</creatorcontrib><creatorcontrib>SU, XIAOJING</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHANG, XUESONG</au><au>CHEN, CHAO</au><au>MA, SHENGZHONG</au><au>WANG, YAN</au><au>ZHANG, XUELIAN</au><au>SU, XIAOJING</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>11</volume><issue>6</issue><spage>4262</spage><epage>4266</epage><pages>4262-4266</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Previous studies have suggested that impairment secondary to mechanical injury is a major cause of irreversible damage to the spinal cord. Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The aim of the present study was to evaluate how changes in the expression levels of the cellular chemokine, monocyte chemoattractant peptide-1 (MCP-1), and the chemotaxis of inflammatory cells (monocytes and macrophages) are involved in the process of SCI. RNA interference methods were used to study the mechanisms that protect residual neurons after SCI in an attempt to explore novel, early interventions for managing SCI. Our results suggested that inhibiting inflammation alleviates nerve cell injury caused by apoptosis and provides a potentially important approach for the future treatment of secondary SCI.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25672988</pmid><doi>10.3892/mmr.2015.3330</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2015-06, Vol.11 (6), p.4262-4266 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Apoptosis Apoptosis - genetics Caspase 3 - genetics Caspase 3 - metabolism Cell injury Chemokine CCL2 - genetics Chemokines Chemotaxis Development and progression Gangrene Gene Expression Regulation Inflammation Inflammation - genetics Inflammation - pathology Macrophages Male monocyte chemoattractant peptide-1 Monocyte chemoattractant protein 1 Monocytes Neurons - metabolism Neurons - pathology Physiological aspects Proteins Rats RNA Interference RNA, Messenger - genetics RNA, Small Interfering - genetics RNA-mediated interference Rodents secondary spinal cord injury Spinal cord injuries Spinal Cord Injuries - genetics Spinal Cord Injuries - pathology Studies Surgery |
| title | Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury |
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