Valproic acid protects motor neuron death by inhibiting oxidative stress and endoplasmic reticulum stress-mediated cytochrome C release after spinal cord injury
Both oxidative stress and endoplasmic reticulum (ER) stress are known to contribute to secondary injury, ultimately leading to cell death after spinal cord injury (SCI). Here, we showed that valproic acid (VPA) reduced cell death of motor neurons by inhibiting cytochrome c release mediated by oxidat...
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description | Both oxidative stress and endoplasmic reticulum (ER) stress are known to contribute to secondary injury, ultimately leading to cell death after spinal cord injury (SCI). Here, we showed that valproic acid (VPA) reduced cell death of motor neurons by inhibiting cytochrome c release mediated by oxidative stress and ER stress after SCI. After SCI, rats were immediately injected with VPA (300 mg/kg) subcutaneously and further injected every 12 h for an indicated time period. Motor neuron cell death at an early time after SCI was significantly attenuated by VPA treatment. Superoxide anion (O2-) production and inducible NO synthase (iNOS) expression linked to oxidative stress was increased after injury, which was inhibited by VPA. In addition, VPA inhibited c-Jun N-terminal kinase (JNK) activation, which was activated and peaked at an early time after SCI. Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. VPA also inhibited cytochrome c release and caspase-9 activation, which was significantly inhibited by SP600125, a JNK inhibitor. The levels of phosphorylated Bim and Mcl-1, which are known as downstream targets of JNK, were significantly reduced by SP600125. On the other hand, VPA treatment inhibited ER stress-induced caspase-12 activation, which is activated in motor neurons after SCI. In addition, VPA increased the Bcl-2/Bax ratio and inhibited CHOP expression. Taken together, our results suggest that cell death of motor neurons after SCI is mediated through oxidative stress and ER stress-mediated cytochrome c release and VPA-inhibited cytochrome c release by attenuating ROS-induced JNK activation followed by Mcl-1 and Bim phosphorylation and ER stress-coupled CHOP expression. |
doi_str_mv | 10.1089/neu.2013.3146 |
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Here, we showed that valproic acid (VPA) reduced cell death of motor neurons by inhibiting cytochrome c release mediated by oxidative stress and ER stress after SCI. After SCI, rats were immediately injected with VPA (300 mg/kg) subcutaneously and further injected every 12 h for an indicated time period. Motor neuron cell death at an early time after SCI was significantly attenuated by VPA treatment. Superoxide anion (O2-) production and inducible NO synthase (iNOS) expression linked to oxidative stress was increased after injury, which was inhibited by VPA. In addition, VPA inhibited c-Jun N-terminal kinase (JNK) activation, which was activated and peaked at an early time after SCI. Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. VPA also inhibited cytochrome c release and caspase-9 activation, which was significantly inhibited by SP600125, a JNK inhibitor. The levels of phosphorylated Bim and Mcl-1, which are known as downstream targets of JNK, were significantly reduced by SP600125. On the other hand, VPA treatment inhibited ER stress-induced caspase-12 activation, which is activated in motor neurons after SCI. In addition, VPA increased the Bcl-2/Bax ratio and inhibited CHOP expression. Taken together, our results suggest that cell death of motor neurons after SCI is mediated through oxidative stress and ER stress-mediated cytochrome c release and VPA-inhibited cytochrome c release by attenuating ROS-induced JNK activation followed by Mcl-1 and Bim phosphorylation and ER stress-coupled CHOP expression.</description><identifier>ISSN: 0897-7151</identifier><identifier>EISSN: 1557-9042</identifier><identifier>DOI: 10.1089/neu.2013.3146</identifier><identifier>PMID: 24294888</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Animals ; Cell Death - drug effects ; Cellular biology ; Cytochromes c - metabolism ; Drug therapy ; Endoplasmic Reticulum Stress - drug effects ; JNK Mitogen-Activated Protein Kinases - metabolism ; Male ; Motor Neurons - drug effects ; Motor Neurons - metabolism ; Motor Neurons - pathology ; Neurons ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Original ; Oxidative stress ; Oxidative Stress - drug effects ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Rodents ; Spinal cord injuries ; Spinal Cord Injuries - drug therapy ; Spinal Cord Injuries - metabolism ; Spinal Cord Injuries - pathology ; Valproic Acid - pharmacology ; Valproic Acid - therapeutic use</subject><ispartof>Journal of neurotrauma, 2014-03, Vol.31 (6), p.582-594</ispartof><rights>(©) Copyright 2014, Mary Ann Liebert, Inc.</rights><rights>Copyright 2014, Mary Ann Liebert, Inc. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-9ac6c866ff3e7afa8bb9ff80565ff91dec32bfefb71eb3e8b9ac489b95d6bacb3</citedby><cites>FETCH-LOGICAL-c514t-9ac6c866ff3e7afa8bb9ff80565ff91dec32bfefb71eb3e8b9ac489b95d6bacb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24294888$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Jee Y</creatorcontrib><creatorcontrib>Maeng, Sejung</creatorcontrib><creatorcontrib>Kang, So R</creatorcontrib><creatorcontrib>Choi, Hye Y</creatorcontrib><creatorcontrib>Oh, Tae H</creatorcontrib><creatorcontrib>Ju, Bong G</creatorcontrib><creatorcontrib>Yune, Tae Y</creatorcontrib><title>Valproic acid protects motor neuron death by inhibiting oxidative stress and endoplasmic reticulum stress-mediated cytochrome C release after spinal cord injury</title><title>Journal of neurotrauma</title><addtitle>J Neurotrauma</addtitle><description>Both oxidative stress and endoplasmic reticulum (ER) stress are known to contribute to secondary injury, ultimately leading to cell death after spinal cord injury (SCI). Here, we showed that valproic acid (VPA) reduced cell death of motor neurons by inhibiting cytochrome c release mediated by oxidative stress and ER stress after SCI. After SCI, rats were immediately injected with VPA (300 mg/kg) subcutaneously and further injected every 12 h for an indicated time period. Motor neuron cell death at an early time after SCI was significantly attenuated by VPA treatment. Superoxide anion (O2-) production and inducible NO synthase (iNOS) expression linked to oxidative stress was increased after injury, which was inhibited by VPA. In addition, VPA inhibited c-Jun N-terminal kinase (JNK) activation, which was activated and peaked at an early time after SCI. Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. VPA also inhibited cytochrome c release and caspase-9 activation, which was significantly inhibited by SP600125, a JNK inhibitor. The levels of phosphorylated Bim and Mcl-1, which are known as downstream targets of JNK, were significantly reduced by SP600125. On the other hand, VPA treatment inhibited ER stress-induced caspase-12 activation, which is activated in motor neurons after SCI. In addition, VPA increased the Bcl-2/Bax ratio and inhibited CHOP expression. Taken together, our results suggest that cell death of motor neurons after SCI is mediated through oxidative stress and ER stress-mediated cytochrome c release and VPA-inhibited cytochrome c release by attenuating ROS-induced JNK activation followed by Mcl-1 and Bim phosphorylation and ER stress-coupled CHOP expression.</description><subject>Animals</subject><subject>Cell Death - drug effects</subject><subject>Cellular biology</subject><subject>Cytochromes c - metabolism</subject><subject>Drug therapy</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Male</subject><subject>Motor Neurons - drug effects</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - pathology</subject><subject>Neurons</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rodents</subject><subject>Spinal cord injuries</subject><subject>Spinal Cord Injuries - drug therapy</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>Spinal Cord Injuries - pathology</subject><subject>Valproic Acid - pharmacology</subject><subject>Valproic Acid - therapeutic use</subject><issn>0897-7151</issn><issn>1557-9042</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNqNkkuPFCEURitG47SjS7eGxI2baoviUbAxMR1fySRu1C3hcZmmU1WUQE2m_40_VdppJ-rKFST3cLgXvqZ5jrst7oR8PcO67TtMtgRT_qDZYMaGVna0f9hsan1oB8zwRfMk50NXMd4Pj5uLnvaSCiE2zY9velxSDBZpGxyq2wK2ZDTFEhOq8hRn5ECXPTJHFOZ9MKGE-RrF2-B0CTeAckmQM9KzQzC7uIw6T9WXoAS7jut0BtoJXNAFHLLHEu0-xQnQrmIj6AxI-wIJ5SXMekQ2JlcvO6zp-LR55PWY4dl5vWy-vn_3Zfexvfr84dPu7VVrGaalldpyKzj3nsCgvRbGSO9FxzjzXmIHlvTGgzcDBkNAmHqACmkkc9xoa8hl8-bOu6ymdmphLkmPaklh0umoog7q78oc9uo63igiqWQdr4JXZ0GK31fIRU0hWxhHPUNcs8KMEikF5cN_oB0fhCSSVfTlP-ghrqm-0S-KEUwIxZVq7yibYs4J_H3fuFOnmKj6k-oUE3WKSeVf_DnsPf07F-QnEfm_rg</recordid><startdate>20140315</startdate><enddate>20140315</enddate><creator>Lee, Jee Y</creator><creator>Maeng, Sejung</creator><creator>Kang, So R</creator><creator>Choi, Hye Y</creator><creator>Oh, Tae H</creator><creator>Ju, Bong G</creator><creator>Yune, Tae Y</creator><general>Mary Ann Liebert, Inc</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>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140315</creationdate><title>Valproic acid protects motor neuron death by inhibiting oxidative stress and endoplasmic reticulum stress-mediated cytochrome C release after spinal cord injury</title><author>Lee, Jee Y ; Maeng, Sejung ; Kang, So R ; Choi, Hye Y ; Oh, Tae H ; Ju, Bong G ; Yune, Tae Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-9ac6c866ff3e7afa8bb9ff80565ff91dec32bfefb71eb3e8b9ac489b95d6bacb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Cell Death - drug effects</topic><topic>Cellular biology</topic><topic>Cytochromes c - metabolism</topic><topic>Drug therapy</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Male</topic><topic>Motor Neurons - drug effects</topic><topic>Motor Neurons - metabolism</topic><topic>Motor Neurons - pathology</topic><topic>Neurons</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rodents</topic><topic>Spinal cord injuries</topic><topic>Spinal Cord Injuries - drug therapy</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>Spinal Cord Injuries - pathology</topic><topic>Valproic Acid - pharmacology</topic><topic>Valproic Acid - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jee Y</creatorcontrib><creatorcontrib>Maeng, Sejung</creatorcontrib><creatorcontrib>Kang, So R</creatorcontrib><creatorcontrib>Choi, Hye Y</creatorcontrib><creatorcontrib>Oh, Tae H</creatorcontrib><creatorcontrib>Ju, Bong G</creatorcontrib><creatorcontrib>Yune, Tae Y</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>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</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>ProQuest Central Essentials</collection><collection>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurotrauma</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Jee Y</au><au>Maeng, Sejung</au><au>Kang, So R</au><au>Choi, Hye Y</au><au>Oh, Tae H</au><au>Ju, Bong G</au><au>Yune, Tae Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Valproic acid protects motor neuron death by inhibiting oxidative stress and endoplasmic reticulum stress-mediated cytochrome C release after spinal cord injury</atitle><jtitle>Journal of neurotrauma</jtitle><addtitle>J Neurotrauma</addtitle><date>2014-03-15</date><risdate>2014</risdate><volume>31</volume><issue>6</issue><spage>582</spage><epage>594</epage><pages>582-594</pages><issn>0897-7151</issn><eissn>1557-9042</eissn><abstract>Both oxidative stress and endoplasmic reticulum (ER) stress are known to contribute to secondary injury, ultimately leading to cell death after spinal cord injury (SCI). Here, we showed that valproic acid (VPA) reduced cell death of motor neurons by inhibiting cytochrome c release mediated by oxidative stress and ER stress after SCI. After SCI, rats were immediately injected with VPA (300 mg/kg) subcutaneously and further injected every 12 h for an indicated time period. Motor neuron cell death at an early time after SCI was significantly attenuated by VPA treatment. Superoxide anion (O2-) production and inducible NO synthase (iNOS) expression linked to oxidative stress was increased after injury, which was inhibited by VPA. In addition, VPA inhibited c-Jun N-terminal kinase (JNK) activation, which was activated and peaked at an early time after SCI. Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. VPA also inhibited cytochrome c release and caspase-9 activation, which was significantly inhibited by SP600125, a JNK inhibitor. The levels of phosphorylated Bim and Mcl-1, which are known as downstream targets of JNK, were significantly reduced by SP600125. On the other hand, VPA treatment inhibited ER stress-induced caspase-12 activation, which is activated in motor neurons after SCI. In addition, VPA increased the Bcl-2/Bax ratio and inhibited CHOP expression. Taken together, our results suggest that cell death of motor neurons after SCI is mediated through oxidative stress and ER stress-mediated cytochrome c release and VPA-inhibited cytochrome c release by attenuating ROS-induced JNK activation followed by Mcl-1 and Bim phosphorylation and ER stress-coupled CHOP expression.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>24294888</pmid><doi>10.1089/neu.2013.3146</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cell Death - drug effects Cellular biology Cytochromes c - metabolism Drug therapy Endoplasmic Reticulum Stress - drug effects JNK Mitogen-Activated Protein Kinases - metabolism Male Motor Neurons - drug effects Motor Neurons - metabolism Motor Neurons - pathology Neurons Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Original Oxidative stress Oxidative Stress - drug effects Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Rodents Spinal cord injuries Spinal Cord Injuries - drug therapy Spinal Cord Injuries - metabolism Spinal Cord Injuries - pathology Valproic Acid - pharmacology Valproic Acid - therapeutic use |
title | Valproic acid protects motor neuron death by inhibiting oxidative stress and endoplasmic reticulum stress-mediated cytochrome C release after spinal cord injury |
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