Holo-transferrin and thrombin can interact to cause brain damage
Previous studies have suggested that delayed release of hemoglobin degradation products, particularly iron, is involved in intracerebral hemorrhage (ICH)-induced brain injury. However, a recent study found evidence of iron-induced brain injury soon after ICH. This study, therefore, examined whether...
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| Veröffentlicht in: | Stroke (1970) 2005-02, Vol.36 (2), p.348-352 |
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| container_title | Stroke (1970) |
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| creator | NAKAMURA, Takehiro GUOHUA XI PARK, Jung-Weon YA HUA HOFF, Julian T KEEP, Richard F |
| description | Previous studies have suggested that delayed release of hemoglobin degradation products, particularly iron, is involved in intracerebral hemorrhage (ICH)-induced brain injury. However, a recent study found evidence of iron-induced brain injury soon after ICH. This study, therefore, examined whether another iron-containing component of blood, holo-transferrin (holo-Tf), might also induce brain injury either alone or in combination with thrombin, another factor involved in early ICH-induced brain injury.
Male Sprague-Dawley rats received an intracerebral infusion of holo-Tf, apo (noniron-loaded)-Tf, thrombin, or a combination of Tf with thrombin into the right basal ganglia. The rats were euthanized 24 hours later for measurement of brain edema and assessment of DNA damage (single- and double-strand breaks and 8-hydroxyl-2'-deoxyguanosine immunohistochemistry). Iron distribution was examined histochemically.
Holo-Tf, apo-Tf, and the dose of thrombin used (1 U) all failed to induce brain edema when administered alone. However, the combination of holo-Tf with thrombin (but not apo-Tf with thrombin) caused brain edema, DNA damage, and intracellular iron accumulation in the ipsilateral basal ganglia.
These results suggest that in addition to hemoglobin-bound iron, Tf-bound iron may contribute to ICH-induced brain injury and that thrombin may contribute to the latter by facilitating cellular iron uptake. |
| doi_str_mv | 10.1161/01.STR.0000153044.60858.1b |
| format | Article |
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Male Sprague-Dawley rats received an intracerebral infusion of holo-Tf, apo (noniron-loaded)-Tf, thrombin, or a combination of Tf with thrombin into the right basal ganglia. The rats were euthanized 24 hours later for measurement of brain edema and assessment of DNA damage (single- and double-strand breaks and 8-hydroxyl-2'-deoxyguanosine immunohistochemistry). Iron distribution was examined histochemically.
Holo-Tf, apo-Tf, and the dose of thrombin used (1 U) all failed to induce brain edema when administered alone. However, the combination of holo-Tf with thrombin (but not apo-Tf with thrombin) caused brain edema, DNA damage, and intracellular iron accumulation in the ipsilateral basal ganglia.
These results suggest that in addition to hemoglobin-bound iron, Tf-bound iron may contribute to ICH-induced brain injury and that thrombin may contribute to the latter by facilitating cellular iron uptake.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.0000153044.60858.1b</identifier><identifier>PMID: 15637325</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Antigens, Nuclear - metabolism ; Biological and medical sciences ; Brain - metabolism ; Brain - pathology ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Cerebral Hemorrhage ; DNA Damage ; DNA Fragmentation ; DNA Repair ; DNA-Binding Proteins - metabolism ; Hemoglobins - chemistry ; Immunohistochemistry ; In Situ Nick-End Labeling ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Investigative techniques, diagnostic techniques (general aspects) ; Iron - pharmacokinetics ; Ku Autoantigen ; Male ; Medical sciences ; Nervous system ; Neurology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Thrombin - chemistry ; Transferrin - chemistry ; Traumas. Diseases due to physical agents ; Ultrasonic investigative techniques ; Vascular diseases and vascular malformations of the nervous system ; Water - metabolism</subject><ispartof>Stroke (1970), 2005-02, Vol.36 (2), p.348-352</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-be1ff36904d0bb12e6c3aef52be07e3abf4b3161bb3ca2457cbf1d33d7289a413</citedby><cites>FETCH-LOGICAL-c588t-be1ff36904d0bb12e6c3aef52be07e3abf4b3161bb3ca2457cbf1d33d7289a413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16449628$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15637325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NAKAMURA, Takehiro</creatorcontrib><creatorcontrib>GUOHUA XI</creatorcontrib><creatorcontrib>PARK, Jung-Weon</creatorcontrib><creatorcontrib>YA HUA</creatorcontrib><creatorcontrib>HOFF, Julian T</creatorcontrib><creatorcontrib>KEEP, Richard F</creatorcontrib><title>Holo-transferrin and thrombin can interact to cause brain damage</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Previous studies have suggested that delayed release of hemoglobin degradation products, particularly iron, is involved in intracerebral hemorrhage (ICH)-induced brain injury. However, a recent study found evidence of iron-induced brain injury soon after ICH. This study, therefore, examined whether another iron-containing component of blood, holo-transferrin (holo-Tf), might also induce brain injury either alone or in combination with thrombin, another factor involved in early ICH-induced brain injury.
Male Sprague-Dawley rats received an intracerebral infusion of holo-Tf, apo (noniron-loaded)-Tf, thrombin, or a combination of Tf with thrombin into the right basal ganglia. The rats were euthanized 24 hours later for measurement of brain edema and assessment of DNA damage (single- and double-strand breaks and 8-hydroxyl-2'-deoxyguanosine immunohistochemistry). Iron distribution was examined histochemically.
Holo-Tf, apo-Tf, and the dose of thrombin used (1 U) all failed to induce brain edema when administered alone. However, the combination of holo-Tf with thrombin (but not apo-Tf with thrombin) caused brain edema, DNA damage, and intracellular iron accumulation in the ipsilateral basal ganglia.
These results suggest that in addition to hemoglobin-bound iron, Tf-bound iron may contribute to ICH-induced brain injury and that thrombin may contribute to the latter by facilitating cellular iron uptake.</description><subject>Animals</subject><subject>Antigens, Nuclear - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Cerebral Hemorrhage</subject><subject>DNA Damage</subject><subject>DNA Fragmentation</subject><subject>DNA Repair</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Hemoglobins - chemistry</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Iron - pharmacokinetics</subject><subject>Ku Autoantigen</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system</subject><subject>Neurology</subject><subject>Oxidative Stress</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Thrombin - chemistry</subject><subject>Transferrin - chemistry</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Ultrasonic investigative techniques</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Water - metabolism</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1LxDAQhoMo7rr6F6QIemvN5KNtPCmLusKCoOs5JGmilX6sSXvw3xvdwh7NJQzzvBnmCUIXgDOAHK4xZK-blwzHA5xixrIcl7zMQB-gOXDCUpaT8hDNMaYiJUyIGToJ4TPyhJb8GM2A57SghM_R7apv-nTwqgvOel93ieqqZPjwfatjYVSX1N1gvTJDMvSxHoNNtFexV6lWvdtTdORUE-zZdC_Q28P9ZrlK18-PT8u7dWp4WQ6ptuAczQVmFdYaiM0NVdZxoi0uLFXaMU3jclpTowjjhdEOKkqrgpRCMaALdLV7d-v7r9GGQbZ1MLZpVGf7Mci8oCUA5v-CUFAQXLAI3uxA4_sQvHVy6-tW-W8JWP6KlhhkFC33ouWfaAk6hs-nKaNubbWPTmYjcDkBKhjVuGjY1GHP5YyJ-Ev0B927huo</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>NAKAMURA, Takehiro</creator><creator>GUOHUA XI</creator><creator>PARK, Jung-Weon</creator><creator>YA HUA</creator><creator>HOFF, Julian T</creator><creator>KEEP, Richard F</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20050201</creationdate><title>Holo-transferrin and thrombin can interact to cause brain damage</title><author>NAKAMURA, Takehiro ; GUOHUA XI ; PARK, Jung-Weon ; YA HUA ; HOFF, Julian T ; KEEP, Richard F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c588t-be1ff36904d0bb12e6c3aef52be07e3abf4b3161bb3ca2457cbf1d33d7289a413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Antigens, Nuclear - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - pathology</topic><topic>Cerebral Hemorrhage</topic><topic>DNA Damage</topic><topic>DNA Fragmentation</topic><topic>DNA Repair</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Hemoglobins - chemistry</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Iron - pharmacokinetics</topic><topic>Ku Autoantigen</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system</topic><topic>Neurology</topic><topic>Oxidative Stress</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Thrombin - chemistry</topic><topic>Transferrin - chemistry</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Ultrasonic investigative techniques</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Water - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAKAMURA, Takehiro</creatorcontrib><creatorcontrib>GUOHUA XI</creatorcontrib><creatorcontrib>PARK, Jung-Weon</creatorcontrib><creatorcontrib>YA HUA</creatorcontrib><creatorcontrib>HOFF, Julian T</creatorcontrib><creatorcontrib>KEEP, Richard F</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAKAMURA, Takehiro</au><au>GUOHUA XI</au><au>PARK, Jung-Weon</au><au>YA HUA</au><au>HOFF, Julian T</au><au>KEEP, Richard F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Holo-transferrin and thrombin can interact to cause brain damage</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>36</volume><issue>2</issue><spage>348</spage><epage>352</epage><pages>348-352</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Previous studies have suggested that delayed release of hemoglobin degradation products, particularly iron, is involved in intracerebral hemorrhage (ICH)-induced brain injury. However, a recent study found evidence of iron-induced brain injury soon after ICH. This study, therefore, examined whether another iron-containing component of blood, holo-transferrin (holo-Tf), might also induce brain injury either alone or in combination with thrombin, another factor involved in early ICH-induced brain injury.
Male Sprague-Dawley rats received an intracerebral infusion of holo-Tf, apo (noniron-loaded)-Tf, thrombin, or a combination of Tf with thrombin into the right basal ganglia. The rats were euthanized 24 hours later for measurement of brain edema and assessment of DNA damage (single- and double-strand breaks and 8-hydroxyl-2'-deoxyguanosine immunohistochemistry). Iron distribution was examined histochemically.
Holo-Tf, apo-Tf, and the dose of thrombin used (1 U) all failed to induce brain edema when administered alone. However, the combination of holo-Tf with thrombin (but not apo-Tf with thrombin) caused brain edema, DNA damage, and intracellular iron accumulation in the ipsilateral basal ganglia.
These results suggest that in addition to hemoglobin-bound iron, Tf-bound iron may contribute to ICH-induced brain injury and that thrombin may contribute to the latter by facilitating cellular iron uptake.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15637325</pmid><doi>10.1161/01.STR.0000153044.60858.1b</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stroke (1970), 2005-02, Vol.36 (2), p.348-352 |
| issn | 0039-2499 1524-4628 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Animals Antigens, Nuclear - metabolism Biological and medical sciences Brain - metabolism Brain - pathology Brain Injuries - metabolism Brain Injuries - pathology Cerebral Hemorrhage DNA Damage DNA Fragmentation DNA Repair DNA-Binding Proteins - metabolism Hemoglobins - chemistry Immunohistochemistry In Situ Nick-End Labeling Injuries of the nervous system and the skull. Diseases due to physical agents Investigative techniques, diagnostic techniques (general aspects) Iron - pharmacokinetics Ku Autoantigen Male Medical sciences Nervous system Neurology Oxidative Stress Rats Rats, Sprague-Dawley Thrombin - chemistry Transferrin - chemistry Traumas. Diseases due to physical agents Ultrasonic investigative techniques Vascular diseases and vascular malformations of the nervous system Water - metabolism |
| title | Holo-transferrin and thrombin can interact to cause brain damage |
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