Nitric oxide facilitates delivery and mediates improved outcome of autologous bone marrow mononuclear cells in a rodent stroke model
Bone marrow mononuclear cells (MNC) represent an investigational treatment for stroke. The objective of this study was to determine the relevance of vasoactive mediators, generated in response to MNC injection, as factors regulating cerebral perfusion (CP), the biodistribution of MNC, and outcome in...
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| Veröffentlicht in: | PloS one 2012-03, Vol.7 (3), p.e32793-e32793 |
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| creator | Kasam, Mallikarjunarao Yang, Bing Strong, Roger Schaar, Krystal Misra, Vivek Xi, Xiaopei Grotta, James C Aronowski, Jaroslaw Savitz, Sean I |
| description | Bone marrow mononuclear cells (MNC) represent an investigational treatment for stroke. The objective of this study was to determine the relevance of vasoactive mediators, generated in response to MNC injection, as factors regulating cerebral perfusion (CP), the biodistribution of MNC, and outcome in stroke.
Long Evans rats underwent transient middle cerebral artery occlusion. MNC were extracted from the bone marrow at 22 hrs and injected via the internal carotid artery or the femoral vein 2 hours later. CP was measured with MRI or continuous laser Doppler flowmetry. Serum samples were collected to measure vasoactive mediators. Animals were treated with the Nitric Oxide (NO) inhibitor, L-NAME, to establish the relevance of NO-signaling to the effect of MNC. Lesion size, MNC biodistribution, and neurological deficits were assessed.
CP transiently increased in the peri-infarct region within 30 min after injecting MNC compared to saline or fibroblast control. This CP increase corresponded temporarily to serum NO elevation and was abolished by L-NAME. Pre-treatment with L-NAME reduced brain penetration of MNC and prevented MNC from reducing infarct lesion size and neurological deficits.
NO generation in response to MNC may represent a mechanism underlying how MNC enter the brain, reduce lesion size, and improve outcome in ischemic stroke. |
| doi_str_mv | 10.1371/journal.pone.0032793 |
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Long Evans rats underwent transient middle cerebral artery occlusion. MNC were extracted from the bone marrow at 22 hrs and injected via the internal carotid artery or the femoral vein 2 hours later. CP was measured with MRI or continuous laser Doppler flowmetry. Serum samples were collected to measure vasoactive mediators. Animals were treated with the Nitric Oxide (NO) inhibitor, L-NAME, to establish the relevance of NO-signaling to the effect of MNC. Lesion size, MNC biodistribution, and neurological deficits were assessed.
CP transiently increased in the peri-infarct region within 30 min after injecting MNC compared to saline or fibroblast control. This CP increase corresponded temporarily to serum NO elevation and was abolished by L-NAME. Pre-treatment with L-NAME reduced brain penetration of MNC and prevented MNC from reducing infarct lesion size and neurological deficits.
NO generation in response to MNC may represent a mechanism underlying how MNC enter the brain, reduce lesion size, and improve outcome in ischemic stroke.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0032793</identifier><identifier>PMID: 22412926</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Autografts ; Biology ; Bone marrow ; Bone Marrow Transplantation ; Brain ; Brain damage ; Cardiomyocytes ; Carotid arteries ; Carotid artery ; Cerebral blood flow ; Cerebrovascular Circulation - drug effects ; Cytokines ; Disease Models, Animal ; Doppler effect ; Enzyme Inhibitors - pharmacology ; Femur ; Fibroblasts ; Hypoxia ; Ischemia ; Lasers ; Leukocytes (mononuclear) ; Ligands ; Magnetic resonance imaging ; Male ; Medical schools ; Medicine ; Middle age ; Neurological diseases ; Neurology ; NG-Nitroarginine methyl ester ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide ; Nitric Oxide - blood ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - antagonists & inhibitors ; Occlusion ; Patient outcomes ; Perfusion ; Rats ; Rodents ; Signaling ; Stem cells ; Stroke ; Stroke - mortality ; Stroke - therapy ; Time Factors ; Transplantation, Autologous ; Treatment Outcome ; Vasoactive agents ; Veins ; Veins & arteries</subject><ispartof>PloS one, 2012-03, Vol.7 (3), p.e32793-e32793</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Kasam et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Kasam et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c724t-192bf8330052b717d6cc27084c47b236c7cfab6af1d0da6a72c15fa0ae9ece6a3</citedby><cites>FETCH-LOGICAL-c724t-192bf8330052b717d6cc27084c47b236c7cfab6af1d0da6a72c15fa0ae9ece6a3</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/PMC3296739/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296739/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23847,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22412926$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kleinschnitz, Christoph</contributor><creatorcontrib>Kasam, Mallikarjunarao</creatorcontrib><creatorcontrib>Yang, Bing</creatorcontrib><creatorcontrib>Strong, Roger</creatorcontrib><creatorcontrib>Schaar, Krystal</creatorcontrib><creatorcontrib>Misra, Vivek</creatorcontrib><creatorcontrib>Xi, Xiaopei</creatorcontrib><creatorcontrib>Grotta, James C</creatorcontrib><creatorcontrib>Aronowski, Jaroslaw</creatorcontrib><creatorcontrib>Savitz, Sean I</creatorcontrib><title>Nitric oxide facilitates delivery and mediates improved outcome of autologous bone marrow mononuclear cells in a rodent stroke model</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Bone marrow mononuclear cells (MNC) represent an investigational treatment for stroke. The objective of this study was to determine the relevance of vasoactive mediators, generated in response to MNC injection, as factors regulating cerebral perfusion (CP), the biodistribution of MNC, and outcome in stroke.
Long Evans rats underwent transient middle cerebral artery occlusion. MNC were extracted from the bone marrow at 22 hrs and injected via the internal carotid artery or the femoral vein 2 hours later. CP was measured with MRI or continuous laser Doppler flowmetry. Serum samples were collected to measure vasoactive mediators. Animals were treated with the Nitric Oxide (NO) inhibitor, L-NAME, to establish the relevance of NO-signaling to the effect of MNC. Lesion size, MNC biodistribution, and neurological deficits were assessed.
CP transiently increased in the peri-infarct region within 30 min after injecting MNC compared to saline or fibroblast control. This CP increase corresponded temporarily to serum NO elevation and was abolished by L-NAME. Pre-treatment with L-NAME reduced brain penetration of MNC and prevented MNC from reducing infarct lesion size and neurological deficits.
NO generation in response to MNC may represent a mechanism underlying how MNC enter the brain, reduce lesion size, and improve outcome in ischemic stroke.</description><subject>Animals</subject><subject>Autografts</subject><subject>Biology</subject><subject>Bone marrow</subject><subject>Bone Marrow Transplantation</subject><subject>Brain</subject><subject>Brain damage</subject><subject>Cardiomyocytes</subject><subject>Carotid arteries</subject><subject>Carotid artery</subject><subject>Cerebral blood flow</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Doppler effect</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Femur</subject><subject>Fibroblasts</subject><subject>Hypoxia</subject><subject>Ischemia</subject><subject>Lasers</subject><subject>Leukocytes (mononuclear)</subject><subject>Ligands</subject><subject>Magnetic resonance imaging</subject><subject>Male</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Middle age</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>NG-Nitroarginine methyl ester</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - blood</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Occlusion</subject><subject>Patient outcomes</subject><subject>Perfusion</subject><subject>Rats</subject><subject>Rodents</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Stroke</subject><subject>Stroke - mortality</subject><subject>Stroke - therapy</subject><subject>Time Factors</subject><subject>Transplantation, Autologous</subject><subject>Treatment Outcome</subject><subject>Vasoactive agents</subject><subject>Veins</subject><subject>Veins & arteries</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1tv0zAUxyMEYmPwDRBYQuLy0OJLascvSNPEpdLEJG6v1qnttB5O3NlO2d754LhrN7VoQigPiU9-55_zPyenqp4SPCZMkLfnYYg9-PEy9HaMMaNCsnvVIZGMjjjF7P7O80H1KKVzjCes4fxhdUBpTaik_LD6_dnl6DQKl85Y1IJ23mXINiFjvVvZeIWgN6izxl1HXbeMYWUNCkPWobMotAiGHHyYhyGhWSkGdRBj-IW60Id-0N5CRNp6X5J7BCgGY_uMUo7hZ2HLyT-uHrTgk32yvR9V3z-8_3byaXR69nF6cnw60oLWeUQknbUNY8UHnQkiDNeaCtzUuhYzyrgWuoUZh5YYbICDoJpMWsBgpdWWAzuqnm90lz4ktW1gUoRRJoWoCS7EdEOYAOdqGV3xcqUCOHUdCHGuIGZXTCkuG8ZtC7IluJYMGkyF1pg23BBDm6Zovdt-bZiV_uniOoLfE91_07uFmoeVYlRywWQReLUViOFisCmrzqV1J6G3pdlKlpE3shGikK__SRJM1u5qMinoi7_Qu_uwpeZQrLq-DaVCvRZVx7UQZIIxXhc4voMql7Gd0-VXaF2J7yW82UsoTLaXeQ5DSmr69cv_s2c_9tmXO-zCgs-LFPyQXejTPlhvQB1DStG2t-MgWK3X6qYbar1WartWJe3Z7ihvk272iP0Bo-Aexw</recordid><startdate>20120307</startdate><enddate>20120307</enddate><creator>Kasam, Mallikarjunarao</creator><creator>Yang, Bing</creator><creator>Strong, Roger</creator><creator>Schaar, Krystal</creator><creator>Misra, Vivek</creator><creator>Xi, Xiaopei</creator><creator>Grotta, James C</creator><creator>Aronowski, Jaroslaw</creator><creator>Savitz, Sean I</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120307</creationdate><title>Nitric oxide facilitates delivery and mediates improved outcome of autologous bone marrow mononuclear cells in a rodent stroke model</title><author>Kasam, Mallikarjunarao ; Yang, Bing ; Strong, Roger ; Schaar, Krystal ; Misra, Vivek ; Xi, Xiaopei ; Grotta, James C ; Aronowski, Jaroslaw ; Savitz, Sean I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c724t-192bf8330052b717d6cc27084c47b236c7cfab6af1d0da6a72c15fa0ae9ece6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Autografts</topic><topic>Biology</topic><topic>Bone marrow</topic><topic>Bone Marrow Transplantation</topic><topic>Brain</topic><topic>Brain damage</topic><topic>Cardiomyocytes</topic><topic>Carotid arteries</topic><topic>Carotid artery</topic><topic>Cerebral blood flow</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Cytokines</topic><topic>Disease Models, Animal</topic><topic>Doppler effect</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Femur</topic><topic>Fibroblasts</topic><topic>Hypoxia</topic><topic>Ischemia</topic><topic>Lasers</topic><topic>Leukocytes (mononuclear)</topic><topic>Ligands</topic><topic>Magnetic resonance imaging</topic><topic>Male</topic><topic>Medical schools</topic><topic>Medicine</topic><topic>Middle age</topic><topic>Neurological diseases</topic><topic>Neurology</topic><topic>NG-Nitroarginine methyl ester</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - blood</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Occlusion</topic><topic>Patient outcomes</topic><topic>Perfusion</topic><topic>Rats</topic><topic>Rodents</topic><topic>Signaling</topic><topic>Stem cells</topic><topic>Stroke</topic><topic>Stroke - mortality</topic><topic>Stroke - therapy</topic><topic>Time Factors</topic><topic>Transplantation, Autologous</topic><topic>Treatment Outcome</topic><topic>Vasoactive agents</topic><topic>Veins</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kasam, Mallikarjunarao</creatorcontrib><creatorcontrib>Yang, Bing</creatorcontrib><creatorcontrib>Strong, Roger</creatorcontrib><creatorcontrib>Schaar, Krystal</creatorcontrib><creatorcontrib>Misra, Vivek</creatorcontrib><creatorcontrib>Xi, Xiaopei</creatorcontrib><creatorcontrib>Grotta, James C</creatorcontrib><creatorcontrib>Aronowski, Jaroslaw</creatorcontrib><creatorcontrib>Savitz, Sean I</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kasam, Mallikarjunarao</au><au>Yang, Bing</au><au>Strong, Roger</au><au>Schaar, Krystal</au><au>Misra, Vivek</au><au>Xi, Xiaopei</au><au>Grotta, James C</au><au>Aronowski, Jaroslaw</au><au>Savitz, Sean I</au><au>Kleinschnitz, Christoph</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric oxide facilitates delivery and mediates improved outcome of autologous bone marrow mononuclear cells in a rodent stroke model</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-03-07</date><risdate>2012</risdate><volume>7</volume><issue>3</issue><spage>e32793</spage><epage>e32793</epage><pages>e32793-e32793</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Bone marrow mononuclear cells (MNC) represent an investigational treatment for stroke. The objective of this study was to determine the relevance of vasoactive mediators, generated in response to MNC injection, as factors regulating cerebral perfusion (CP), the biodistribution of MNC, and outcome in stroke.
Long Evans rats underwent transient middle cerebral artery occlusion. MNC were extracted from the bone marrow at 22 hrs and injected via the internal carotid artery or the femoral vein 2 hours later. CP was measured with MRI or continuous laser Doppler flowmetry. Serum samples were collected to measure vasoactive mediators. Animals were treated with the Nitric Oxide (NO) inhibitor, L-NAME, to establish the relevance of NO-signaling to the effect of MNC. Lesion size, MNC biodistribution, and neurological deficits were assessed.
CP transiently increased in the peri-infarct region within 30 min after injecting MNC compared to saline or fibroblast control. This CP increase corresponded temporarily to serum NO elevation and was abolished by L-NAME. Pre-treatment with L-NAME reduced brain penetration of MNC and prevented MNC from reducing infarct lesion size and neurological deficits.
NO generation in response to MNC may represent a mechanism underlying how MNC enter the brain, reduce lesion size, and improve outcome in ischemic stroke.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22412926</pmid><doi>10.1371/journal.pone.0032793</doi><tpages>e32793</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-03, Vol.7 (3), p.e32793-e32793 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1323977410 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Animals Autografts Biology Bone marrow Bone Marrow Transplantation Brain Brain damage Cardiomyocytes Carotid arteries Carotid artery Cerebral blood flow Cerebrovascular Circulation - drug effects Cytokines Disease Models, Animal Doppler effect Enzyme Inhibitors - pharmacology Femur Fibroblasts Hypoxia Ischemia Lasers Leukocytes (mononuclear) Ligands Magnetic resonance imaging Male Medical schools Medicine Middle age Neurological diseases Neurology NG-Nitroarginine methyl ester NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Nitric Oxide - blood Nitric Oxide - metabolism Nitric Oxide Synthase - antagonists & inhibitors Occlusion Patient outcomes Perfusion Rats Rodents Signaling Stem cells Stroke Stroke - mortality Stroke - therapy Time Factors Transplantation, Autologous Treatment Outcome Vasoactive agents Veins Veins & arteries |
| title | Nitric oxide facilitates delivery and mediates improved outcome of autologous bone marrow mononuclear cells in a rodent stroke model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T02%3A40%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Nitric%20oxide%20facilitates%20delivery%20and%20mediates%20improved%20outcome%20of%20autologous%20bone%20marrow%20mononuclear%20cells%20in%20a%20rodent%20stroke%20model&rft.jtitle=PloS%20one&rft.au=Kasam,%20Mallikarjunarao&rft.date=2012-03-07&rft.volume=7&rft.issue=3&rft.spage=e32793&rft.epage=e32793&rft.pages=e32793-e32793&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0032793&rft_dat=%3Cgale_plos_%3EA477150009%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1323977410&rft_id=info:pmid/22412926&rft_galeid=A477150009&rft_doaj_id=oai_doaj_org_article_69836efa9f10493a8027cc0286d1d288&rfr_iscdi=true |