The potential role of HO-1 in regulating the MLK3-MKK7-JNK3 module scaffolded by JIP1 during cerebral ischemia/reperfusion in rats
Heme oxygenase (HO-1), which may be induced by Cobaltic protoporphyrin IX chloride (CoPPIX) or Rosiglitazone (Ros), is a neuroprotective agent that effectively reduces ischemic stroke. Previous studies have shown that the neuroprotective mechanisms of HO-1 are related to JNK signaling. The expressio...
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| Veröffentlicht in: | Behavioural brain research 2019-02, Vol.359, p.528-535 |
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| creator | Song, Yuan-Jian Dai, Chun-Xiao Li, Man Cui, Miao-miao Ding, Xin Zhao, Xiao-Fang Wang, Cai-Lin Li, Zhen-Ling Guo, Meng-Yuan Fu, Yan-Yan Wen, Xiang-Ru Qi, Da-Shi Wang, Yu-Lan |
| description | Heme oxygenase (HO-1), which may be induced by Cobaltic protoporphyrin IX chloride (CoPPIX) or Rosiglitazone (Ros), is a neuroprotective agent that effectively reduces ischemic stroke. Previous studies have shown that the neuroprotective mechanisms of HO-1 are related to JNK signaling. The expression of HO-1 protects cells from death through the JNK signaling pathway. This study aimed to ascertain whether the neuroprotective effect of HO-1 depends on the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and further influences the JNK signal transmission through HO-1. Prior to the ischemia-reperfusion experiment, CoPPIX was injected through the lateral ventricle for 5 consecutive days or Ros was administered via intraperitoneal administration in the week prior to transient ischemia. Our results demonstrated that HO-1 could inhibit the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and could ultimately diminish the phosphorylation of JNK3. Furthermore, the inhibition of JNK3 phosphorylation downregulated the level of p-c-Jun and elevated neuronal cell death in the CA1 of the hippocampus. Taken together, these findings suggested that HO-1 could ameliorate brain injury by regulating the MLK3-MKK7-JNK3 signaling module, which was scaffolded by JIP1 and JNK signaling during cerebral ischemia/reperfusion. |
| doi_str_mv | 10.1016/j.bbr.2018.11.003 |
| format | Article |
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Previous studies have shown that the neuroprotective mechanisms of HO-1 are related to JNK signaling. The expression of HO-1 protects cells from death through the JNK signaling pathway. This study aimed to ascertain whether the neuroprotective effect of HO-1 depends on the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and further influences the JNK signal transmission through HO-1. Prior to the ischemia-reperfusion experiment, CoPPIX was injected through the lateral ventricle for 5 consecutive days or Ros was administered via intraperitoneal administration in the week prior to transient ischemia. Our results demonstrated that HO-1 could inhibit the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and could ultimately diminish the phosphorylation of JNK3. Furthermore, the inhibition of JNK3 phosphorylation downregulated the level of p-c-Jun and elevated neuronal cell death in the CA1 of the hippocampus. Taken together, these findings suggested that HO-1 could ameliorate brain injury by regulating the MLK3-MKK7-JNK3 signaling module, which was scaffolded by JIP1 and JNK signaling during cerebral ischemia/reperfusion.</description><identifier>ISSN: 0166-4328</identifier><identifier>EISSN: 1872-7549</identifier><identifier>DOI: 10.1016/j.bbr.2018.11.003</identifier><identifier>PMID: 30412737</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Adaptor Proteins, Signal Transducing - metabolism ; Animals ; Brain Ischemia - drug therapy ; Brain Ischemia - enzymology ; Brain Ischemia - pathology ; CA1 Region, Hippocampal - drug effects ; CA1 Region, Hippocampal - enzymology ; CA1 Region, Hippocampal - pathology ; Cell Death - physiology ; Disease Models, Animal ; Down-Regulation ; Heme Oxygenase (Decyclizing) - metabolism ; HO-1 ; ischemia/reperfusion ; JIP1 ; JNK3 ; Male ; MAP Kinase Kinase Kinases - metabolism ; Maze Learning - drug effects ; Maze Learning - physiology ; Mitogen-Activated Protein Kinase 10 - metabolism ; Mitogen-Activated Protein Kinase Kinase Kinase 11 ; Mitogen-Activated Protein Kinases - metabolism ; MLK3-MKK7-JNK3 ; Neurons - drug effects ; Neurons - enzymology ; Neurons - pathology ; Neuroprotection - drug effects ; Neuroprotection - physiology ; Neuroprotective Agents - pharmacology ; Phosphorylation ; Proto-Oncogene Proteins c-jun - metabolism ; Rats, Sprague-Dawley ; Reperfusion Injury - drug therapy ; Reperfusion Injury - enzymology ; Reperfusion Injury - pathology ; Rosiglitazone - pharmacology</subject><ispartof>Behavioural brain research, 2019-02, Vol.359, p.528-535</ispartof><rights>2018 Elsevier B.V.</rights><rights>Copyright © 2018 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c353t-4242d4bcdcc6cdcff7cc4376a2308069d0ad9661505c7797c4d867a7489a24213</citedby><cites>FETCH-LOGICAL-c353t-4242d4bcdcc6cdcff7cc4376a2308069d0ad9661505c7797c4d867a7489a24213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0166432818302201$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30412737$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, Yuan-Jian</creatorcontrib><creatorcontrib>Dai, Chun-Xiao</creatorcontrib><creatorcontrib>Li, Man</creatorcontrib><creatorcontrib>Cui, Miao-miao</creatorcontrib><creatorcontrib>Ding, Xin</creatorcontrib><creatorcontrib>Zhao, Xiao-Fang</creatorcontrib><creatorcontrib>Wang, Cai-Lin</creatorcontrib><creatorcontrib>Li, Zhen-Ling</creatorcontrib><creatorcontrib>Guo, Meng-Yuan</creatorcontrib><creatorcontrib>Fu, Yan-Yan</creatorcontrib><creatorcontrib>Wen, Xiang-Ru</creatorcontrib><creatorcontrib>Qi, Da-Shi</creatorcontrib><creatorcontrib>Wang, Yu-Lan</creatorcontrib><title>The potential role of HO-1 in regulating the MLK3-MKK7-JNK3 module scaffolded by JIP1 during cerebral ischemia/reperfusion in rats</title><title>Behavioural brain research</title><addtitle>Behav Brain Res</addtitle><description>Heme oxygenase (HO-1), which may be induced by Cobaltic protoporphyrin IX chloride (CoPPIX) or Rosiglitazone (Ros), is a neuroprotective agent that effectively reduces ischemic stroke. Previous studies have shown that the neuroprotective mechanisms of HO-1 are related to JNK signaling. The expression of HO-1 protects cells from death through the JNK signaling pathway. This study aimed to ascertain whether the neuroprotective effect of HO-1 depends on the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and further influences the JNK signal transmission through HO-1. Prior to the ischemia-reperfusion experiment, CoPPIX was injected through the lateral ventricle for 5 consecutive days or Ros was administered via intraperitoneal administration in the week prior to transient ischemia. Our results demonstrated that HO-1 could inhibit the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and could ultimately diminish the phosphorylation of JNK3. Furthermore, the inhibition of JNK3 phosphorylation downregulated the level of p-c-Jun and elevated neuronal cell death in the CA1 of the hippocampus. Taken together, these findings suggested that HO-1 could ameliorate brain injury by regulating the MLK3-MKK7-JNK3 signaling module, which was scaffolded by JIP1 and JNK signaling during cerebral ischemia/reperfusion.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - enzymology</subject><subject>Brain Ischemia - pathology</subject><subject>CA1 Region, Hippocampal - drug effects</subject><subject>CA1 Region, Hippocampal - enzymology</subject><subject>CA1 Region, Hippocampal - pathology</subject><subject>Cell Death - physiology</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Heme Oxygenase (Decyclizing) - metabolism</subject><subject>HO-1</subject><subject>ischemia/reperfusion</subject><subject>JIP1</subject><subject>JNK3</subject><subject>Male</subject><subject>MAP Kinase Kinase Kinases - metabolism</subject><subject>Maze Learning - drug effects</subject><subject>Maze Learning - physiology</subject><subject>Mitogen-Activated Protein Kinase 10 - metabolism</subject><subject>Mitogen-Activated Protein Kinase Kinase Kinase 11</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>MLK3-MKK7-JNK3</subject><subject>Neurons - drug effects</subject><subject>Neurons - enzymology</subject><subject>Neurons - pathology</subject><subject>Neuroprotection - drug effects</subject><subject>Neuroprotection - physiology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-jun - metabolism</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - enzymology</subject><subject>Reperfusion Injury - pathology</subject><subject>Rosiglitazone - pharmacology</subject><issn>0166-4328</issn><issn>1872-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kD9v1DAYhy0Eao_SD8CCPLIk9Ws7cSImVAFt7_pnKLPl2G9an5L4sBOkrnxyfFzbkcVent8j-yHkI7ASGNRn27LrYskZNCVAyZh4Q1bQKF6oSrZvySozdSEFb47J-5S2jDHJKjgix4JJ4EqoFflz_4h0F2acZm8GGsOANPT04rYA6ica8WEZzOynBzpn8HqzFsX1eq2Kq5u1oGNwS-aTNX0fBoeOdk_06vIOqFvifmMxYhez1yf7iKM3ZxF3GPsl-TD985s5fSDvejMkPH2-T8jP79_uzy-Kze2Py_Ovm8KKSsyF5JI72VlnbZ2PvlfWSqFqwwVrWN06Zlxb11CxyirVKitdUyujZNOaPAVxQj4fvLsYfi2YZj3mZ-EwmAnDknRGOBeglMgoHFAbQ0oRe72LfjTxSQPT-_R6q3N6vU-vAXROnzefnvVLN6J7Xby0zsCXA4D5k789Rp2sx8mi8xHtrF3w_9H_Bdi-koI</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Song, Yuan-Jian</creator><creator>Dai, Chun-Xiao</creator><creator>Li, Man</creator><creator>Cui, Miao-miao</creator><creator>Ding, Xin</creator><creator>Zhao, Xiao-Fang</creator><creator>Wang, Cai-Lin</creator><creator>Li, Zhen-Ling</creator><creator>Guo, Meng-Yuan</creator><creator>Fu, Yan-Yan</creator><creator>Wen, Xiang-Ru</creator><creator>Qi, Da-Shi</creator><creator>Wang, Yu-Lan</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></search><sort><creationdate>20190201</creationdate><title>The potential role of HO-1 in regulating the MLK3-MKK7-JNK3 module scaffolded by JIP1 during cerebral ischemia/reperfusion in rats</title><author>Song, Yuan-Jian ; Dai, Chun-Xiao ; Li, Man ; Cui, Miao-miao ; Ding, Xin ; Zhao, Xiao-Fang ; Wang, Cai-Lin ; Li, Zhen-Ling ; Guo, Meng-Yuan ; Fu, Yan-Yan ; Wen, Xiang-Ru ; Qi, Da-Shi ; Wang, Yu-Lan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c353t-4242d4bcdcc6cdcff7cc4376a2308069d0ad9661505c7797c4d867a7489a24213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Animals</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - enzymology</topic><topic>Brain Ischemia - pathology</topic><topic>CA1 Region, Hippocampal - drug effects</topic><topic>CA1 Region, Hippocampal - enzymology</topic><topic>CA1 Region, Hippocampal - pathology</topic><topic>Cell Death - physiology</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Heme Oxygenase (Decyclizing) - metabolism</topic><topic>HO-1</topic><topic>ischemia/reperfusion</topic><topic>JIP1</topic><topic>JNK3</topic><topic>Male</topic><topic>MAP Kinase Kinase Kinases - metabolism</topic><topic>Maze Learning - drug effects</topic><topic>Maze Learning - physiology</topic><topic>Mitogen-Activated Protein Kinase 10 - metabolism</topic><topic>Mitogen-Activated Protein Kinase Kinase Kinase 11</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>MLK3-MKK7-JNK3</topic><topic>Neurons - drug effects</topic><topic>Neurons - enzymology</topic><topic>Neurons - pathology</topic><topic>Neuroprotection - drug effects</topic><topic>Neuroprotection - physiology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-jun - metabolism</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - enzymology</topic><topic>Reperfusion Injury - pathology</topic><topic>Rosiglitazone - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Yuan-Jian</creatorcontrib><creatorcontrib>Dai, Chun-Xiao</creatorcontrib><creatorcontrib>Li, Man</creatorcontrib><creatorcontrib>Cui, Miao-miao</creatorcontrib><creatorcontrib>Ding, Xin</creatorcontrib><creatorcontrib>Zhao, Xiao-Fang</creatorcontrib><creatorcontrib>Wang, Cai-Lin</creatorcontrib><creatorcontrib>Li, Zhen-Ling</creatorcontrib><creatorcontrib>Guo, Meng-Yuan</creatorcontrib><creatorcontrib>Fu, Yan-Yan</creatorcontrib><creatorcontrib>Wen, Xiang-Ru</creatorcontrib><creatorcontrib>Qi, Da-Shi</creatorcontrib><creatorcontrib>Wang, Yu-Lan</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><jtitle>Behavioural brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Yuan-Jian</au><au>Dai, Chun-Xiao</au><au>Li, Man</au><au>Cui, Miao-miao</au><au>Ding, Xin</au><au>Zhao, Xiao-Fang</au><au>Wang, Cai-Lin</au><au>Li, Zhen-Ling</au><au>Guo, Meng-Yuan</au><au>Fu, Yan-Yan</au><au>Wen, Xiang-Ru</au><au>Qi, Da-Shi</au><au>Wang, Yu-Lan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The potential role of HO-1 in regulating the MLK3-MKK7-JNK3 module scaffolded by JIP1 during cerebral ischemia/reperfusion in rats</atitle><jtitle>Behavioural brain research</jtitle><addtitle>Behav Brain Res</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>359</volume><spage>528</spage><epage>535</epage><pages>528-535</pages><issn>0166-4328</issn><eissn>1872-7549</eissn><abstract>Heme oxygenase (HO-1), which may be induced by Cobaltic protoporphyrin IX chloride (CoPPIX) or Rosiglitazone (Ros), is a neuroprotective agent that effectively reduces ischemic stroke. Previous studies have shown that the neuroprotective mechanisms of HO-1 are related to JNK signaling. The expression of HO-1 protects cells from death through the JNK signaling pathway. This study aimed to ascertain whether the neuroprotective effect of HO-1 depends on the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and further influences the JNK signal transmission through HO-1. Prior to the ischemia-reperfusion experiment, CoPPIX was injected through the lateral ventricle for 5 consecutive days or Ros was administered via intraperitoneal administration in the week prior to transient ischemia. Our results demonstrated that HO-1 could inhibit the assembly of the MLK3-MKK7-JNK3 signaling module scaffolded by JIP1 and could ultimately diminish the phosphorylation of JNK3. Furthermore, the inhibition of JNK3 phosphorylation downregulated the level of p-c-Jun and elevated neuronal cell death in the CA1 of the hippocampus. Taken together, these findings suggested that HO-1 could ameliorate brain injury by regulating the MLK3-MKK7-JNK3 signaling module, which was scaffolded by JIP1 and JNK signaling during cerebral ischemia/reperfusion.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>30412737</pmid><doi>10.1016/j.bbr.2018.11.003</doi><tpages>8</tpages></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - metabolism Animals Brain Ischemia - drug therapy Brain Ischemia - enzymology Brain Ischemia - pathology CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - enzymology CA1 Region, Hippocampal - pathology Cell Death - physiology Disease Models, Animal Down-Regulation Heme Oxygenase (Decyclizing) - metabolism HO-1 ischemia/reperfusion JIP1 JNK3 Male MAP Kinase Kinase Kinases - metabolism Maze Learning - drug effects Maze Learning - physiology Mitogen-Activated Protein Kinase 10 - metabolism Mitogen-Activated Protein Kinase Kinase Kinase 11 Mitogen-Activated Protein Kinases - metabolism MLK3-MKK7-JNK3 Neurons - drug effects Neurons - enzymology Neurons - pathology Neuroprotection - drug effects Neuroprotection - physiology Neuroprotective Agents - pharmacology Phosphorylation Proto-Oncogene Proteins c-jun - metabolism Rats, Sprague-Dawley Reperfusion Injury - drug therapy Reperfusion Injury - enzymology Reperfusion Injury - pathology Rosiglitazone - pharmacology |
| title | The potential role of HO-1 in regulating the MLK3-MKK7-JNK3 module scaffolded by JIP1 during cerebral ischemia/reperfusion in rats |
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