Inducible nitric oxide synthase expression in human cerebral infarcts
The inducible or "immunological" isoform of nitric oxide synthase (iNOS) is induced in many cell types by inflammatory stimuli and synthesizes toxic amounts of NO. In rodent models of focal cerebral ischemia, iNOS is expressed in neutrophils invading the injured brain and in local blood ve...
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| Veröffentlicht in: | Acta neuropathologica 1999-03, Vol.97 (3), p.215-220 |
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| creator | FORSTER, C CLARK, H. B ROSS, M. E IADECOLA, C |
| description | The inducible or "immunological" isoform of nitric oxide synthase (iNOS) is induced in many cell types by inflammatory stimuli and synthesizes toxic amounts of NO. In rodent models of focal cerebral ischemia, iNOS is expressed in neutrophils invading the injured brain and in local blood vessels. Studies with iNOS inhibitors and iNOS null mice indicate that NO produced by iNOS contributes to ischemic brain injury. In the present study, we sought to determine whether iNOS is also expressed in the human brain after ischemic stroke. Studies were conducted using immunohistochemistry on autopsy brains with neuropathological evidence of acute cerebral infarction. iNOS immunoreactivity was observed in neutrophils infiltrating the ischemic brain and in blood vessels within the ischemic territory. iNOS-positive cells also were immunoreactive for nitrotyrosine, reflecting protein nitration by NO-derived peroxynitrite and nitrites. iNOS or nitrotyrosine immunoreactivity was not detected outside the region of the infarct. These observations provide evidence that iNOS is expressed in the human brain after ischemic infarction and support the hypothesis that iNOS inhibitors may be useful in the treatment of ischemic stroke in humans. |
| doi_str_mv | 10.1007/s004010050977 |
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B ; ROSS, M. E ; IADECOLA, C</creator><creatorcontrib>FORSTER, C ; CLARK, H. B ; ROSS, M. E ; IADECOLA, C</creatorcontrib><description>The inducible or "immunological" isoform of nitric oxide synthase (iNOS) is induced in many cell types by inflammatory stimuli and synthesizes toxic amounts of NO. In rodent models of focal cerebral ischemia, iNOS is expressed in neutrophils invading the injured brain and in local blood vessels. Studies with iNOS inhibitors and iNOS null mice indicate that NO produced by iNOS contributes to ischemic brain injury. In the present study, we sought to determine whether iNOS is also expressed in the human brain after ischemic stroke. Studies were conducted using immunohistochemistry on autopsy brains with neuropathological evidence of acute cerebral infarction. iNOS immunoreactivity was observed in neutrophils infiltrating the ischemic brain and in blood vessels within the ischemic territory. iNOS-positive cells also were immunoreactive for nitrotyrosine, reflecting protein nitration by NO-derived peroxynitrite and nitrites. iNOS or nitrotyrosine immunoreactivity was not detected outside the region of the infarct. These observations provide evidence that iNOS is expressed in the human brain after ischemic infarction and support the hypothesis that iNOS inhibitors may be useful in the treatment of ischemic stroke in humans.</description><identifier>ISSN: 0001-6322</identifier><identifier>EISSN: 1432-0533</identifier><identifier>DOI: 10.1007/s004010050977</identifier><identifier>PMID: 10090667</identifier><identifier>CODEN: ANPTAL</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Aged ; Aged, 80 and over ; Animal models ; Autopsy ; Biological and medical sciences ; Blood vessels ; Blood Vessels - enzymology ; Brain ; Brain injury ; Cerebral infarction ; Cerebral Infarction - enzymology ; Eosinophils - enzymology ; Female ; Humans ; Immunohistochemistry ; Inflammation ; Ischemia ; Leukocytes (neutrophilic) ; Male ; Medical sciences ; Middle Aged ; Necrosis ; Neurology ; Neurons - pathology ; Neutrophils ; Neutrophils - enzymology ; Nitration ; Nitric oxide ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase Type II ; Nitric-oxide synthase ; Nitrites ; Nitrotyrosine ; Peroxynitrite ; Rodents ; Stroke ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Acta neuropathologica, 1999-03, Vol.97 (3), p.215-220</ispartof><rights>1999 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 1999.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-fc65e630c9b905e10d130325105a24d4bdb1d54483aa1409aa668f032e13ea363</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1792794$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10090667$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FORSTER, C</creatorcontrib><creatorcontrib>CLARK, H. B</creatorcontrib><creatorcontrib>ROSS, M. E</creatorcontrib><creatorcontrib>IADECOLA, C</creatorcontrib><title>Inducible nitric oxide synthase expression in human cerebral infarcts</title><title>Acta neuropathologica</title><addtitle>Acta Neuropathol</addtitle><description>The inducible or "immunological" isoform of nitric oxide synthase (iNOS) is induced in many cell types by inflammatory stimuli and synthesizes toxic amounts of NO. In rodent models of focal cerebral ischemia, iNOS is expressed in neutrophils invading the injured brain and in local blood vessels. Studies with iNOS inhibitors and iNOS null mice indicate that NO produced by iNOS contributes to ischemic brain injury. In the present study, we sought to determine whether iNOS is also expressed in the human brain after ischemic stroke. Studies were conducted using immunohistochemistry on autopsy brains with neuropathological evidence of acute cerebral infarction. iNOS immunoreactivity was observed in neutrophils infiltrating the ischemic brain and in blood vessels within the ischemic territory. iNOS-positive cells also were immunoreactive for nitrotyrosine, reflecting protein nitration by NO-derived peroxynitrite and nitrites. iNOS or nitrotyrosine immunoreactivity was not detected outside the region of the infarct. These observations provide evidence that iNOS is expressed in the human brain after ischemic infarction and support the hypothesis that iNOS inhibitors may be useful in the treatment of ischemic stroke in humans.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Animal models</subject><subject>Autopsy</subject><subject>Biological and medical sciences</subject><subject>Blood vessels</subject><subject>Blood Vessels - enzymology</subject><subject>Brain</subject><subject>Brain injury</subject><subject>Cerebral infarction</subject><subject>Cerebral Infarction - enzymology</subject><subject>Eosinophils - enzymology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Leukocytes (neutrophilic)</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Necrosis</subject><subject>Neurology</subject><subject>Neurons - pathology</subject><subject>Neutrophils</subject><subject>Neutrophils - enzymology</subject><subject>Nitration</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitric-oxide synthase</subject><subject>Nitrites</subject><subject>Nitrotyrosine</subject><subject>Peroxynitrite</subject><subject>Rodents</subject><subject>Stroke</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0001-6322</issn><issn>1432-0533</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</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>eNpV0E1Lw0AQBuBFFBurR68S0Gt09rs5SqlaKHjRc9hsJnRLuqm7CbT_3pUW1NN88DADLyG3FB4pgH6KAAJSJ6HU-oxkVHBWgOT8nGQAQAvFGZuQqxg3aWJayEsySb4EpXRGFkvfjNbVHebeDcHZvN-7BvN48MPaRMxxvwsYo-t97ny-HrfG5xYD1sF0adOaYId4TS5a00W8OdUp-XxZfMzfitX763L-vCqsoGwoWqskKg62rEuQSKGhHDiTFKRhohF1U9NGCjHjxlABpTFKzdokkHI0XPEpuT_e3YX-a8Q4VJt-DD69rJigUlMNkiVVHJUNfYwB22oX3NaEQ0Wh-gmt-hda8nenq2O9xeaPPqaUwMMJmGhN1wbjrYu_TpdMl4J_A_x-chc</recordid><startdate>19990301</startdate><enddate>19990301</enddate><creator>FORSTER, C</creator><creator>CLARK, H. 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| subjects | Aged Aged, 80 and over Animal models Autopsy Biological and medical sciences Blood vessels Blood Vessels - enzymology Brain Brain injury Cerebral infarction Cerebral Infarction - enzymology Eosinophils - enzymology Female Humans Immunohistochemistry Inflammation Ischemia Leukocytes (neutrophilic) Male Medical sciences Middle Aged Necrosis Neurology Neurons - pathology Neutrophils Neutrophils - enzymology Nitration Nitric oxide Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase Type II Nitric-oxide synthase Nitrites Nitrotyrosine Peroxynitrite Rodents Stroke Vascular diseases and vascular malformations of the nervous system |
| title | Inducible nitric oxide synthase expression in human cerebral infarcts |
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