Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury
The transient receptor potential melastatin 4 (TRPM4) channel has been suggested to play a key role in the treatment of ischemic stroke. However, in vivo evaluation of TRPM4 channel, in particular by direct channel suppression, is lacking. In this study, we used multimodal imaging to assess edema fo...
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| Veröffentlicht in: | Translational stroke research 2019-02, Vol.10 (1), p.91-103 |
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| creator | Chen, Bo Ng, Gandi Gao, Yahui Low, See Wee Sandanaraj, Edwin Ramasamy, Boominathan Sekar, Sakthivel Bhakoo, Kishore Soong, Tuck Wah Nilius, Bernd Tang, Carol Robins, Edward G. Goggi, Julian Liao, Ping |
| description | The transient receptor potential melastatin 4 (TRPM4) channel has been suggested to play a key role in the treatment of ischemic stroke. However, in vivo evaluation of TRPM4 channel, in particular by direct channel suppression, is lacking. In this study, we used multimodal imaging to assess edema formation and quantify the amount of metabolically functional brain salvaged after a rat model of stroke reperfusion. TRPM4 upregulation in endothelium emerges as early as 2 h post-stroke induction. Expression of TRPM4 channel was suppressed directly in vivo by treatment with siRNA; scrambled siRNA was used as a control. T2-weighted MRI suggests that TRPM4 inhibition successfully reduces edema by 30% and concomitantly salvages functionally active brain, measured by
18
F-FDG-PET. These in vivo imaging results correlate well with post-mortem 2,3,5-triphenyltetrazolium chloride (TTC) staining which exhibits a 34.9% reduction in infarct volume after siRNA treatment. Furthermore, in a permanent stroke model, large areas of brain tissue displayed both edema and significant reductions in metabolic activity which was not shown in transient models with or without TRPM4 inhibition, indicating that tissue salvaged by TRPM4 inhibition during stroke reperfusion may survive. Evans Blue extravasation and hemoglobin quantification in the ipsilateral hemisphere were greatly reduced, suggesting that TRPM4 inhibition can improve BBB integrity after ischemic stroke reperfusion. Our results support the use of TRPM4 blocker for early stroke reperfusion. |
| doi_str_mv | 10.1007/s12975-018-0621-3 |
| format | Article |
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18
F-FDG-PET. These in vivo imaging results correlate well with post-mortem 2,3,5-triphenyltetrazolium chloride (TTC) staining which exhibits a 34.9% reduction in infarct volume after siRNA treatment. Furthermore, in a permanent stroke model, large areas of brain tissue displayed both edema and significant reductions in metabolic activity which was not shown in transient models with or without TRPM4 inhibition, indicating that tissue salvaged by TRPM4 inhibition during stroke reperfusion may survive. Evans Blue extravasation and hemoglobin quantification in the ipsilateral hemisphere were greatly reduced, suggesting that TRPM4 inhibition can improve BBB integrity after ischemic stroke reperfusion. Our results support the use of TRPM4 blocker for early stroke reperfusion.</description><identifier>ISSN: 1868-4483</identifier><identifier>EISSN: 1868-601X</identifier><identifier>DOI: 10.1007/s12975-018-0621-3</identifier><identifier>PMID: 29569041</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Blood-brain barrier ; Blood-Brain Barrier - pathology ; Blood-Brain Barrier - physiopathology ; Brain ; Brain Edema ; Cardiology ; Disease Models, Animal ; Edema ; Fluorodeoxyglucose F18 - pharmacokinetics ; Functional Laterality ; Gene Expression Regulation - physiology ; Hemoglobin ; Image Processing, Computer-Assisted ; Infarction, Middle Cerebral Artery - complications ; Infarction, Middle Cerebral Artery - drug therapy ; Ischemia ; Magnetic resonance imaging ; Male ; Microarray Analysis ; Multimodal Imaging - methods ; Neurology ; Neurosciences ; Neurosurgery ; Original ; Original Article ; Phosphopyruvate Hydratase - metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury - complications ; Reperfusion Injury - drug therapy ; RNA, Messenger - metabolism ; RNA, Small Interfering - therapeutic use ; Stroke ; TRPM Cation Channels - antagonists & inhibitors ; TRPM Cation Channels - genetics ; TRPM Cation Channels - metabolism ; Vascular Surgery ; von Willebrand Factor - metabolism</subject><ispartof>Translational stroke research, 2019-02, Vol.10 (1), p.91-103</ispartof><rights>The Author(s) 2018</rights><rights>The Author(s) 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-3ed4986554a15b54e23111c7b39e78dc19d36db72d3c08a009339805378184283</citedby><cites>FETCH-LOGICAL-c470t-3ed4986554a15b54e23111c7b39e78dc19d36db72d3c08a009339805378184283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12975-018-0621-3$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2919608228?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,315,781,785,886,21393,21394,27929,27930,33535,33536,33749,33750,41493,42562,43664,43810,51324,64390,64392,64394,72474</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29569041$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Bo</creatorcontrib><creatorcontrib>Ng, Gandi</creatorcontrib><creatorcontrib>Gao, Yahui</creatorcontrib><creatorcontrib>Low, See Wee</creatorcontrib><creatorcontrib>Sandanaraj, Edwin</creatorcontrib><creatorcontrib>Ramasamy, Boominathan</creatorcontrib><creatorcontrib>Sekar, Sakthivel</creatorcontrib><creatorcontrib>Bhakoo, Kishore</creatorcontrib><creatorcontrib>Soong, Tuck Wah</creatorcontrib><creatorcontrib>Nilius, Bernd</creatorcontrib><creatorcontrib>Tang, Carol</creatorcontrib><creatorcontrib>Robins, Edward G.</creatorcontrib><creatorcontrib>Goggi, Julian</creatorcontrib><creatorcontrib>Liao, Ping</creatorcontrib><title>Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury</title><title>Translational stroke research</title><addtitle>Transl. Stroke Res</addtitle><addtitle>Transl Stroke Res</addtitle><description>The transient receptor potential melastatin 4 (TRPM4) channel has been suggested to play a key role in the treatment of ischemic stroke. However, in vivo evaluation of TRPM4 channel, in particular by direct channel suppression, is lacking. In this study, we used multimodal imaging to assess edema formation and quantify the amount of metabolically functional brain salvaged after a rat model of stroke reperfusion. TRPM4 upregulation in endothelium emerges as early as 2 h post-stroke induction. Expression of TRPM4 channel was suppressed directly in vivo by treatment with siRNA; scrambled siRNA was used as a control. T2-weighted MRI suggests that TRPM4 inhibition successfully reduces edema by 30% and concomitantly salvages functionally active brain, measured by
18
F-FDG-PET. These in vivo imaging results correlate well with post-mortem 2,3,5-triphenyltetrazolium chloride (TTC) staining which exhibits a 34.9% reduction in infarct volume after siRNA treatment. Furthermore, in a permanent stroke model, large areas of brain tissue displayed both edema and significant reductions in metabolic activity which was not shown in transient models with or without TRPM4 inhibition, indicating that tissue salvaged by TRPM4 inhibition during stroke reperfusion may survive. Evans Blue extravasation and hemoglobin quantification in the ipsilateral hemisphere were greatly reduced, suggesting that TRPM4 inhibition can improve BBB integrity after ischemic stroke reperfusion. Our results support the use of TRPM4 blocker for early stroke reperfusion.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - pathology</subject><subject>Blood-Brain Barrier - physiopathology</subject><subject>Brain</subject><subject>Brain Edema</subject><subject>Cardiology</subject><subject>Disease Models, Animal</subject><subject>Edema</subject><subject>Fluorodeoxyglucose F18 - pharmacokinetics</subject><subject>Functional Laterality</subject><subject>Gene Expression Regulation - physiology</subject><subject>Hemoglobin</subject><subject>Image Processing, Computer-Assisted</subject><subject>Infarction, Middle Cerebral Artery - complications</subject><subject>Infarction, Middle Cerebral Artery - drug therapy</subject><subject>Ischemia</subject><subject>Magnetic resonance imaging</subject><subject>Male</subject><subject>Microarray Analysis</subject><subject>Multimodal Imaging - methods</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Original</subject><subject>Original Article</subject><subject>Phosphopyruvate Hydratase - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - drug therapy</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering - therapeutic use</subject><subject>Stroke</subject><subject>TRPM Cation Channels - antagonists & inhibitors</subject><subject>TRPM Cation Channels - genetics</subject><subject>TRPM Cation Channels - metabolism</subject><subject>Vascular Surgery</subject><subject>von Willebrand Factor - metabolism</subject><issn>1868-4483</issn><issn>1868-601X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU9v1DAQxS0EolXbD8AFWeLCJcVjO_5zQaoKlEgtRW2RuFlO4t31kthbO1m0354suy0UCV9s6b35zYwfQq-AnAIh8l0GqmVZEFAFERQK9gwdghKqEAS-P9-_OVfsAJ3kvCTTYcAFZy_RAdWl0ITDIVp8iaGowtpmv3b4auwG38fWdn7Y4Kq3cx_m-INPrhm6Db5dxJ8Z3918veK4Cgtf-8HHgM961_mY7OAyvh1S_OHwjVu5NBvzVq7CckybY_RiZrvsTvb3Efr26ePd-efi8vqiOj-7LBouyVAw13KtRFlyC2VdckcZADSyZtpJ1TagWybaWtKWNURZQjRjWpGSSQWKU8WO0PsddzXWvWsbF4ZkO7NKvrdpY6L15qkS_MLM49oIRiUhW8DbPSDF-9HlwfQ-N67rbHBxzIZOP05AgtST9c0_1mUcU5jWM1SDFkTR3xPBztWkmHNys8dhgJhtlGYXpZnAZhulYVPN67-3eKx4CG4y0J0hT1KYu_Sn9f-pvwC6FKkw</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Chen, Bo</creator><creator>Ng, Gandi</creator><creator>Gao, Yahui</creator><creator>Low, See Wee</creator><creator>Sandanaraj, Edwin</creator><creator>Ramasamy, Boominathan</creator><creator>Sekar, Sakthivel</creator><creator>Bhakoo, Kishore</creator><creator>Soong, Tuck Wah</creator><creator>Nilius, Bernd</creator><creator>Tang, Carol</creator><creator>Robins, Edward G.</creator><creator>Goggi, Julian</creator><creator>Liao, Ping</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><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>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190201</creationdate><title>Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury</title><author>Chen, Bo ; Ng, Gandi ; Gao, Yahui ; Low, See Wee ; Sandanaraj, Edwin ; Ramasamy, Boominathan ; Sekar, Sakthivel ; Bhakoo, Kishore ; Soong, Tuck Wah ; Nilius, Bernd ; Tang, Carol ; Robins, Edward G. ; Goggi, Julian ; Liao, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-3ed4986554a15b54e23111c7b39e78dc19d36db72d3c08a009339805378184283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - pathology</topic><topic>Blood-Brain Barrier - physiopathology</topic><topic>Brain</topic><topic>Brain Edema</topic><topic>Cardiology</topic><topic>Disease Models, Animal</topic><topic>Edema</topic><topic>Fluorodeoxyglucose F18 - pharmacokinetics</topic><topic>Functional Laterality</topic><topic>Gene Expression Regulation - physiology</topic><topic>Hemoglobin</topic><topic>Image Processing, Computer-Assisted</topic><topic>Infarction, Middle Cerebral Artery - complications</topic><topic>Infarction, Middle Cerebral Artery - drug therapy</topic><topic>Ischemia</topic><topic>Magnetic resonance imaging</topic><topic>Male</topic><topic>Microarray Analysis</topic><topic>Multimodal Imaging - methods</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Original</topic><topic>Original Article</topic><topic>Phosphopyruvate Hydratase - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - drug therapy</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering - therapeutic use</topic><topic>Stroke</topic><topic>TRPM Cation Channels - antagonists & inhibitors</topic><topic>TRPM Cation Channels - genetics</topic><topic>TRPM Cation Channels - metabolism</topic><topic>Vascular Surgery</topic><topic>von Willebrand Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Bo</creatorcontrib><creatorcontrib>Ng, Gandi</creatorcontrib><creatorcontrib>Gao, Yahui</creatorcontrib><creatorcontrib>Low, See Wee</creatorcontrib><creatorcontrib>Sandanaraj, Edwin</creatorcontrib><creatorcontrib>Ramasamy, Boominathan</creatorcontrib><creatorcontrib>Sekar, Sakthivel</creatorcontrib><creatorcontrib>Bhakoo, Kishore</creatorcontrib><creatorcontrib>Soong, Tuck Wah</creatorcontrib><creatorcontrib>Nilius, Bernd</creatorcontrib><creatorcontrib>Tang, Carol</creatorcontrib><creatorcontrib>Robins, Edward G.</creatorcontrib><creatorcontrib>Goggi, Julian</creatorcontrib><creatorcontrib>Liao, Ping</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><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>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</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>Health & Medical Collection (Alumni Edition)</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 One Psychology</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Translational stroke research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Bo</au><au>Ng, Gandi</au><au>Gao, Yahui</au><au>Low, See Wee</au><au>Sandanaraj, Edwin</au><au>Ramasamy, Boominathan</au><au>Sekar, Sakthivel</au><au>Bhakoo, Kishore</au><au>Soong, Tuck Wah</au><au>Nilius, Bernd</au><au>Tang, Carol</au><au>Robins, Edward G.</au><au>Goggi, Julian</au><au>Liao, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury</atitle><jtitle>Translational stroke research</jtitle><stitle>Transl. Stroke Res</stitle><addtitle>Transl Stroke Res</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>10</volume><issue>1</issue><spage>91</spage><epage>103</epage><pages>91-103</pages><issn>1868-4483</issn><eissn>1868-601X</eissn><abstract>The transient receptor potential melastatin 4 (TRPM4) channel has been suggested to play a key role in the treatment of ischemic stroke. However, in vivo evaluation of TRPM4 channel, in particular by direct channel suppression, is lacking. In this study, we used multimodal imaging to assess edema formation and quantify the amount of metabolically functional brain salvaged after a rat model of stroke reperfusion. TRPM4 upregulation in endothelium emerges as early as 2 h post-stroke induction. Expression of TRPM4 channel was suppressed directly in vivo by treatment with siRNA; scrambled siRNA was used as a control. T2-weighted MRI suggests that TRPM4 inhibition successfully reduces edema by 30% and concomitantly salvages functionally active brain, measured by
18
F-FDG-PET. These in vivo imaging results correlate well with post-mortem 2,3,5-triphenyltetrazolium chloride (TTC) staining which exhibits a 34.9% reduction in infarct volume after siRNA treatment. Furthermore, in a permanent stroke model, large areas of brain tissue displayed both edema and significant reductions in metabolic activity which was not shown in transient models with or without TRPM4 inhibition, indicating that tissue salvaged by TRPM4 inhibition during stroke reperfusion may survive. Evans Blue extravasation and hemoglobin quantification in the ipsilateral hemisphere were greatly reduced, suggesting that TRPM4 inhibition can improve BBB integrity after ischemic stroke reperfusion. Our results support the use of TRPM4 blocker for early stroke reperfusion.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29569041</pmid><doi>10.1007/s12975-018-0621-3</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Translational stroke research, 2019-02, Vol.10 (1), p.91-103 |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Blood-brain barrier Blood-Brain Barrier - pathology Blood-Brain Barrier - physiopathology Brain Brain Edema Cardiology Disease Models, Animal Edema Fluorodeoxyglucose F18 - pharmacokinetics Functional Laterality Gene Expression Regulation - physiology Hemoglobin Image Processing, Computer-Assisted Infarction, Middle Cerebral Artery - complications Infarction, Middle Cerebral Artery - drug therapy Ischemia Magnetic resonance imaging Male Microarray Analysis Multimodal Imaging - methods Neurology Neurosciences Neurosurgery Original Original Article Phosphopyruvate Hydratase - metabolism Rats Rats, Wistar Reperfusion Injury - complications Reperfusion Injury - drug therapy RNA, Messenger - metabolism RNA, Small Interfering - therapeutic use Stroke TRPM Cation Channels - antagonists & inhibitors TRPM Cation Channels - genetics TRPM Cation Channels - metabolism Vascular Surgery von Willebrand Factor - metabolism |
| title | Non-Invasive Multimodality Imaging Directly Shows TRPM4 Inhibition Ameliorates Stroke Reperfusion Injury |
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