Complement activation associates with saccular cerebral artery aneurysm wall degeneration and rupture
Saccular cerebral artery aneurysm (SCAA) wall degeneration and inflammatory cell infiltrations associate with aneurysm rupture and subarachnoid hemorrhage, resulting in a devastating form of stroke. The complement system is the key mediator of inflammation and household processing of injured tissue....
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| Veröffentlicht in: | Neurosurgery 2006-11, Vol.59 (5), p.1069-1077 |
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| creator | Tulamo, Riikka Frösen, Juhana Junnikkala, Sami Paetau, Anders Pitkäniemi, Janne Kangasniemi, Marko Niemelä, Mika Jääskeläinen, Juha Jokitalo, Eija Karatas, Ayse Hernesniemi, Juha Meri, Seppo |
| description | Saccular cerebral artery aneurysm (SCAA) wall degeneration and inflammatory cell infiltrations associate with aneurysm rupture and subarachnoid hemorrhage, resulting in a devastating form of stroke. The complement system is the key mediator of inflammation and household processing of injured tissue. We studied how complement activation associates with SCAA wall degeneration and rupture to better understand the pathobiology of SCAA wall rupture.
Unruptured (n = 26) and ruptured (n = 32) SCAA fundi resected after microsurgical clipping were studied by immunostaining for complement activation (membrane attack complex [MAC]) and by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling reaction for related cell death. Complement activation was correlated with clinical and other histological parameters. Electromicroscopy and immunoelectron microscopy were used for locating MAC depositions at the ultrastructural level.
MAC localized consistently in a decellularized layer in the outer SCAA wall, and was found in all SCAA samples. The percentage of MAC-positive area relative to the total SCAA wall surface area (range, 5-77%) was greater in ruptured (n = 25; median, 39%) than in unruptured SCAAs (n = 18; median, 20%; P = 0.005). It also associated significantly with SCAA wall degeneration (P < 0.001), de-endothelialization(P < 0.001), and CD163+ macrophage (P = 0.023) and T-lymphocyte (P = 0.030) infiltrations. Apoptotic terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling-positive nuclei and MAC were located at the same wall areas in four out of 14 double-stained samples, but no double-positive cells were found. Electromicroscopy and immunoelectron microscopy of an unruptured SCAA showed cell death in the MAC-positive layers in the outer SCAA wall.
These data suggests that complement activation and MAC formation are involved in SCAA wall degeneration and rupture. |
| doi_str_mv | 10.1227/01.NEU.0000245598.84698.26 |
| format | Article |
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Unruptured (n = 26) and ruptured (n = 32) SCAA fundi resected after microsurgical clipping were studied by immunostaining for complement activation (membrane attack complex [MAC]) and by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling reaction for related cell death. Complement activation was correlated with clinical and other histological parameters. Electromicroscopy and immunoelectron microscopy were used for locating MAC depositions at the ultrastructural level.
MAC localized consistently in a decellularized layer in the outer SCAA wall, and was found in all SCAA samples. The percentage of MAC-positive area relative to the total SCAA wall surface area (range, 5-77%) was greater in ruptured (n = 25; median, 39%) than in unruptured SCAAs (n = 18; median, 20%; P = 0.005). It also associated significantly with SCAA wall degeneration (P < 0.001), de-endothelialization(P < 0.001), and CD163+ macrophage (P = 0.023) and T-lymphocyte (P = 0.030) infiltrations. Apoptotic terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling-positive nuclei and MAC were located at the same wall areas in four out of 14 double-stained samples, but no double-positive cells were found. Electromicroscopy and immunoelectron microscopy of an unruptured SCAA showed cell death in the MAC-positive layers in the outer SCAA wall.
These data suggests that complement activation and MAC formation are involved in SCAA wall degeneration and rupture.</description><identifier>ISSN: 0148-396X</identifier><identifier>EISSN: 1524-4040</identifier><identifier>DOI: 10.1227/01.NEU.0000245598.84698.26</identifier><identifier>PMID: 17016232</identifier><language>eng</language><publisher>United States</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cerebral Arterial Diseases - immunology ; Cerebral Arterial Diseases - pathology ; Complement Activation - immunology ; Female ; Humans ; Intracranial Aneurysm - immunology ; Intracranial Aneurysm - pathology ; Male ; Middle Aged ; Statistics as Topic</subject><ispartof>Neurosurgery, 2006-11, Vol.59 (5), p.1069-1077</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c304t-d059f08595d7c21818e53e79c96207a201db48d10bc6532e0c817f0d8c8cc56d3</citedby><cites>FETCH-LOGICAL-c304t-d059f08595d7c21818e53e79c96207a201db48d10bc6532e0c817f0d8c8cc56d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17016232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tulamo, Riikka</creatorcontrib><creatorcontrib>Frösen, Juhana</creatorcontrib><creatorcontrib>Junnikkala, Sami</creatorcontrib><creatorcontrib>Paetau, Anders</creatorcontrib><creatorcontrib>Pitkäniemi, Janne</creatorcontrib><creatorcontrib>Kangasniemi, Marko</creatorcontrib><creatorcontrib>Niemelä, Mika</creatorcontrib><creatorcontrib>Jääskeläinen, Juha</creatorcontrib><creatorcontrib>Jokitalo, Eija</creatorcontrib><creatorcontrib>Karatas, Ayse</creatorcontrib><creatorcontrib>Hernesniemi, Juha</creatorcontrib><creatorcontrib>Meri, Seppo</creatorcontrib><title>Complement activation associates with saccular cerebral artery aneurysm wall degeneration and rupture</title><title>Neurosurgery</title><addtitle>Neurosurgery</addtitle><description>Saccular cerebral artery aneurysm (SCAA) wall degeneration and inflammatory cell infiltrations associate with aneurysm rupture and subarachnoid hemorrhage, resulting in a devastating form of stroke. The complement system is the key mediator of inflammation and household processing of injured tissue. We studied how complement activation associates with SCAA wall degeneration and rupture to better understand the pathobiology of SCAA wall rupture.
Unruptured (n = 26) and ruptured (n = 32) SCAA fundi resected after microsurgical clipping were studied by immunostaining for complement activation (membrane attack complex [MAC]) and by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling reaction for related cell death. Complement activation was correlated with clinical and other histological parameters. Electromicroscopy and immunoelectron microscopy were used for locating MAC depositions at the ultrastructural level.
MAC localized consistently in a decellularized layer in the outer SCAA wall, and was found in all SCAA samples. The percentage of MAC-positive area relative to the total SCAA wall surface area (range, 5-77%) was greater in ruptured (n = 25; median, 39%) than in unruptured SCAAs (n = 18; median, 20%; P = 0.005). It also associated significantly with SCAA wall degeneration (P < 0.001), de-endothelialization(P < 0.001), and CD163+ macrophage (P = 0.023) and T-lymphocyte (P = 0.030) infiltrations. Apoptotic terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling-positive nuclei and MAC were located at the same wall areas in four out of 14 double-stained samples, but no double-positive cells were found. Electromicroscopy and immunoelectron microscopy of an unruptured SCAA showed cell death in the MAC-positive layers in the outer SCAA wall.
These data suggests that complement activation and MAC formation are involved in SCAA wall degeneration and rupture.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Cerebral Arterial Diseases - immunology</subject><subject>Cerebral Arterial Diseases - pathology</subject><subject>Complement Activation - immunology</subject><subject>Female</subject><subject>Humans</subject><subject>Intracranial Aneurysm - immunology</subject><subject>Intracranial Aneurysm - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Statistics as Topic</subject><issn>0148-396X</issn><issn>1524-4040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LAzEQhoMotlb_ggQP3rZOskk2601K_YCiFwveQppMdWU_apK19N-72oJzmJnD-74zPIRcMZgyzosbYNPn-XIKQ3EhZamnWqihc3VExkxykQkQcEzGwITO8lK9jchZjJ8ATIlCn5IRK4aV53xMcNY1mxobbBO1LlXfNlVdS22Mnatswki3Vfqg0TrX1zZQhwFXwdbUhoRhR22LfdjFhm5tXVOP79hiOGS0noZ-k_qA5-RkbeuIF4c5Icv7-evsMVu8PDzN7haZy0GkzIMs16BlKX3hONNMo8yxKF2pOBSWA_MroT2DlVMy5whOs2INXjvtnFQ-n5Drfe4mdF89xmSaKjqs6-HNro9Gac6AgxyEt3uhC12MAddmE6rGhp1hYH4hG2BmgGz-IZs_yIarwXx5uNKvGvT_1gPV_AfvEHqF</recordid><startdate>200611</startdate><enddate>200611</enddate><creator>Tulamo, Riikka</creator><creator>Frösen, Juhana</creator><creator>Junnikkala, Sami</creator><creator>Paetau, Anders</creator><creator>Pitkäniemi, Janne</creator><creator>Kangasniemi, Marko</creator><creator>Niemelä, Mika</creator><creator>Jääskeläinen, Juha</creator><creator>Jokitalo, Eija</creator><creator>Karatas, Ayse</creator><creator>Hernesniemi, Juha</creator><creator>Meri, Seppo</creator><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>200611</creationdate><title>Complement activation associates with saccular cerebral artery aneurysm wall degeneration and rupture</title><author>Tulamo, Riikka ; Frösen, Juhana ; Junnikkala, Sami ; Paetau, Anders ; Pitkäniemi, Janne ; Kangasniemi, Marko ; Niemelä, Mika ; Jääskeläinen, Juha ; Jokitalo, Eija ; Karatas, Ayse ; Hernesniemi, Juha ; Meri, Seppo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c304t-d059f08595d7c21818e53e79c96207a201db48d10bc6532e0c817f0d8c8cc56d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Cerebral Arterial Diseases - immunology</topic><topic>Cerebral Arterial Diseases - pathology</topic><topic>Complement Activation - immunology</topic><topic>Female</topic><topic>Humans</topic><topic>Intracranial Aneurysm - immunology</topic><topic>Intracranial Aneurysm - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Statistics as Topic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tulamo, Riikka</creatorcontrib><creatorcontrib>Frösen, Juhana</creatorcontrib><creatorcontrib>Junnikkala, Sami</creatorcontrib><creatorcontrib>Paetau, Anders</creatorcontrib><creatorcontrib>Pitkäniemi, Janne</creatorcontrib><creatorcontrib>Kangasniemi, Marko</creatorcontrib><creatorcontrib>Niemelä, Mika</creatorcontrib><creatorcontrib>Jääskeläinen, Juha</creatorcontrib><creatorcontrib>Jokitalo, Eija</creatorcontrib><creatorcontrib>Karatas, Ayse</creatorcontrib><creatorcontrib>Hernesniemi, Juha</creatorcontrib><creatorcontrib>Meri, Seppo</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>Neurosurgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tulamo, Riikka</au><au>Frösen, Juhana</au><au>Junnikkala, Sami</au><au>Paetau, Anders</au><au>Pitkäniemi, Janne</au><au>Kangasniemi, Marko</au><au>Niemelä, Mika</au><au>Jääskeläinen, Juha</au><au>Jokitalo, Eija</au><au>Karatas, Ayse</au><au>Hernesniemi, Juha</au><au>Meri, Seppo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complement activation associates with saccular cerebral artery aneurysm wall degeneration and rupture</atitle><jtitle>Neurosurgery</jtitle><addtitle>Neurosurgery</addtitle><date>2006-11</date><risdate>2006</risdate><volume>59</volume><issue>5</issue><spage>1069</spage><epage>1077</epage><pages>1069-1077</pages><issn>0148-396X</issn><eissn>1524-4040</eissn><abstract>Saccular cerebral artery aneurysm (SCAA) wall degeneration and inflammatory cell infiltrations associate with aneurysm rupture and subarachnoid hemorrhage, resulting in a devastating form of stroke. The complement system is the key mediator of inflammation and household processing of injured tissue. We studied how complement activation associates with SCAA wall degeneration and rupture to better understand the pathobiology of SCAA wall rupture.
Unruptured (n = 26) and ruptured (n = 32) SCAA fundi resected after microsurgical clipping were studied by immunostaining for complement activation (membrane attack complex [MAC]) and by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling reaction for related cell death. Complement activation was correlated with clinical and other histological parameters. Electromicroscopy and immunoelectron microscopy were used for locating MAC depositions at the ultrastructural level.
MAC localized consistently in a decellularized layer in the outer SCAA wall, and was found in all SCAA samples. The percentage of MAC-positive area relative to the total SCAA wall surface area (range, 5-77%) was greater in ruptured (n = 25; median, 39%) than in unruptured SCAAs (n = 18; median, 20%; P = 0.005). It also associated significantly with SCAA wall degeneration (P < 0.001), de-endothelialization(P < 0.001), and CD163+ macrophage (P = 0.023) and T-lymphocyte (P = 0.030) infiltrations. Apoptotic terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling-positive nuclei and MAC were located at the same wall areas in four out of 14 double-stained samples, but no double-positive cells were found. Electromicroscopy and immunoelectron microscopy of an unruptured SCAA showed cell death in the MAC-positive layers in the outer SCAA wall.
These data suggests that complement activation and MAC formation are involved in SCAA wall degeneration and rupture.</abstract><cop>United States</cop><pmid>17016232</pmid><doi>10.1227/01.NEU.0000245598.84698.26</doi><tpages>9</tpages></addata></record> |
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| ispartof | Neurosurgery, 2006-11, Vol.59 (5), p.1069-1077 |
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| subjects | Adolescent Adult Aged Aged, 80 and over Cerebral Arterial Diseases - immunology Cerebral Arterial Diseases - pathology Complement Activation - immunology Female Humans Intracranial Aneurysm - immunology Intracranial Aneurysm - pathology Male Middle Aged Statistics as Topic |
| title | Complement activation associates with saccular cerebral artery aneurysm wall degeneration and rupture |
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