Apoptosis and cell proliferation after porcine coronary angioplasty
Angioplasty initiates a number of responses in the vessel wall including cellular migration, proliferation, and matrix accumulation, all of which contribute to neointima formation and restenosis. Cellular homeostasis within a tissue depends on the balance between cell proliferation and apoptosis. Pr...
Gespeichert in:
| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1998-10, Vol.98 (16), p.1657-1665 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1665 |
|---|---|
| container_issue | 16 |
| container_start_page | 1657 |
| container_title | Circulation (New York, N.Y.) |
| container_volume | 98 |
| creator | MALIK, N FRANCIS, S. E HOLT, C. M GUNN, J THOMAS, G. L SHEPHERD, L CHAMBERLAIN, J NEWMAN, C. M. H CUMBERLAND, D. C CROSSMAN, D. C |
| description | Angioplasty initiates a number of responses in the vessel wall including cellular migration, proliferation, and matrix accumulation, all of which contribute to neointima formation and restenosis. Cellular homeostasis within a tissue depends on the balance between cell proliferation and apoptosis.
Profiles of apoptosis and proliferation were therefore examined in a porcine PTCA injury model over a 28-day period. Forty-two arteries from 21 pigs, harvested at the site of maximal injury at 1, 6, and 18 hours, and 3, 7, 14, and 28 days after PTCA, were examined (n=3 animals per time point). Uninjured arteries were used as controls. Apoptosis was demonstrated by the terminal uridine nick-end labeling (TUNEL) method, transmission electron microscopy (TEM), and DNA fragmentation. Cells traversing the cell cycle were identified by immunostaining for proliferating cell nuclear antigen (PCNA). Apoptosis was not detected in control vessels at all time points nor at 28 days after PTCA. Apoptotic cells were identified at all early time points with a peak at 6 hours (5.1+/-0.26%; compared to uninjured artery, P |
| doi_str_mv | 10.1161/01.cir.98.16.1657 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69965161</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69965161</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-c3fe69207a2712125486ed5b57244a6584cb8154465f6cb07cd27673f618af913</originalsourceid><addsrcrecordid>eNpdkE1LAzEQhoMotVZ_gAdhEfG2NZPPzbEUPwoFQfQc0jSRlO1mTbaH_ntTLD0IA8Mwz8y88yJ0C3gKIOAJw9SGNFXNFEQJLs_QGDhhNeNUnaMxxljVkhJyia5y3pRSUMlHaKSkbCglYzSf9bEfYg65Mt26sq5tqz7FNniXzBBiVxk_uFT1MdnQucrGFDuT9oX-DrFvTR721-jCmza7m2OeoK-X58_5W718f13MZ8vackyH2lLvhCJYGiKBAOGsEW7NV1wSxozgDbOrBjhjgnthV1jaNZFCUi-gMV4BnaDHv71F4M_O5UFvQz4oNp2Lu6yFUoIXWwp4_w_cxF3qijZd7kpCqGQFgj_Ipphzcl73KWzLaxqwPrirMej54kOrRoPQB3fLzN1x8W61devTxNHO0n849k22pvXJdDbkE0YYkRQo_QXpyID6</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>212722374</pqid></control><display><type>article</type><title>Apoptosis and cell proliferation after porcine coronary angioplasty</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Journals@Ovid Complete</source><creator>MALIK, N ; FRANCIS, S. E ; HOLT, C. M ; GUNN, J ; THOMAS, G. L ; SHEPHERD, L ; CHAMBERLAIN, J ; NEWMAN, C. M. H ; CUMBERLAND, D. C ; CROSSMAN, D. C</creator><creatorcontrib>MALIK, N ; FRANCIS, S. E ; HOLT, C. M ; GUNN, J ; THOMAS, G. L ; SHEPHERD, L ; CHAMBERLAIN, J ; NEWMAN, C. M. H ; CUMBERLAND, D. C ; CROSSMAN, D. C</creatorcontrib><description>Angioplasty initiates a number of responses in the vessel wall including cellular migration, proliferation, and matrix accumulation, all of which contribute to neointima formation and restenosis. Cellular homeostasis within a tissue depends on the balance between cell proliferation and apoptosis.
Profiles of apoptosis and proliferation were therefore examined in a porcine PTCA injury model over a 28-day period. Forty-two arteries from 21 pigs, harvested at the site of maximal injury at 1, 6, and 18 hours, and 3, 7, 14, and 28 days after PTCA, were examined (n=3 animals per time point). Uninjured arteries were used as controls. Apoptosis was demonstrated by the terminal uridine nick-end labeling (TUNEL) method, transmission electron microscopy (TEM), and DNA fragmentation. Cells traversing the cell cycle were identified by immunostaining for proliferating cell nuclear antigen (PCNA). Apoptosis was not detected in control vessels at all time points nor at 28 days after PTCA. Apoptotic cells were identified at all early time points with a peak at 6 hours (5.1+/-0.26%; compared to uninjured artery, P<0.001) and confirmed by characteristic DNA ladders and TEM findings. Regional analysis showed apoptosis within the media, adventitia, and neointima peaked at 18 hours, 6 hours, and 7 days after PTCA, respectively. In comparison, PCNA staining peaked at 3 days after PTCA (7.16+/-0.29%; compared to 1.78+/-0.08% PCNA-positive cells in the uninjured artery, P<0.001). Profiles of apoptosis and cell proliferation after PTCA were discordant in all layers of the artery except the neointima. These profiles also differed between traumatized and nontraumatized regions of the arterial wall. Immunostaining with cell-type specific markers and TEM analysis revealed that apoptotic cells included vascular smooth muscle cells (VSMCs), inflammatory cells, and adventitial fibroblasts.
These results suggest that the profile of apoptosis and proliferation after PTCA is regional and cell specific, and attempts to modulate either of these events for therapeutic benefit requires recognition of these differences.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.98.16.1657</identifier><identifier>PMID: 9778332</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Actins - analysis ; Angioplasty, Balloon, Coronary - adverse effects ; Animals ; Antigens - analysis ; Apoptosis - physiology ; Biological and medical sciences ; Cell Division - physiology ; Cell Nucleus - ultrastructure ; Coronary Vessels - injuries ; Diseases of the cardiovascular system ; In Situ Nick-End Labeling ; Logistic Models ; Medical sciences ; Microscopy, Electron ; Muscle, Smooth, Vascular - immunology ; Muscle, Smooth, Vascular - ultrastructure ; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) ; Staining and Labeling ; Swine</subject><ispartof>Circulation (New York, N.Y.), 1998-10, Vol.98 (16), p.1657-1665</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Oct 20, 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-c3fe69207a2712125486ed5b57244a6584cb8154465f6cb07cd27673f618af913</citedby><cites>FETCH-LOGICAL-c503t-c3fe69207a2712125486ed5b57244a6584cb8154465f6cb07cd27673f618af913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,3689,27931,27932</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2427313$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9778332$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MALIK, N</creatorcontrib><creatorcontrib>FRANCIS, S. E</creatorcontrib><creatorcontrib>HOLT, C. M</creatorcontrib><creatorcontrib>GUNN, J</creatorcontrib><creatorcontrib>THOMAS, G. L</creatorcontrib><creatorcontrib>SHEPHERD, L</creatorcontrib><creatorcontrib>CHAMBERLAIN, J</creatorcontrib><creatorcontrib>NEWMAN, C. M. H</creatorcontrib><creatorcontrib>CUMBERLAND, D. C</creatorcontrib><creatorcontrib>CROSSMAN, D. C</creatorcontrib><title>Apoptosis and cell proliferation after porcine coronary angioplasty</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Angioplasty initiates a number of responses in the vessel wall including cellular migration, proliferation, and matrix accumulation, all of which contribute to neointima formation and restenosis. Cellular homeostasis within a tissue depends on the balance between cell proliferation and apoptosis.
Profiles of apoptosis and proliferation were therefore examined in a porcine PTCA injury model over a 28-day period. Forty-two arteries from 21 pigs, harvested at the site of maximal injury at 1, 6, and 18 hours, and 3, 7, 14, and 28 days after PTCA, were examined (n=3 animals per time point). Uninjured arteries were used as controls. Apoptosis was demonstrated by the terminal uridine nick-end labeling (TUNEL) method, transmission electron microscopy (TEM), and DNA fragmentation. Cells traversing the cell cycle were identified by immunostaining for proliferating cell nuclear antigen (PCNA). Apoptosis was not detected in control vessels at all time points nor at 28 days after PTCA. Apoptotic cells were identified at all early time points with a peak at 6 hours (5.1+/-0.26%; compared to uninjured artery, P<0.001) and confirmed by characteristic DNA ladders and TEM findings. Regional analysis showed apoptosis within the media, adventitia, and neointima peaked at 18 hours, 6 hours, and 7 days after PTCA, respectively. In comparison, PCNA staining peaked at 3 days after PTCA (7.16+/-0.29%; compared to 1.78+/-0.08% PCNA-positive cells in the uninjured artery, P<0.001). Profiles of apoptosis and cell proliferation after PTCA were discordant in all layers of the artery except the neointima. These profiles also differed between traumatized and nontraumatized regions of the arterial wall. Immunostaining with cell-type specific markers and TEM analysis revealed that apoptotic cells included vascular smooth muscle cells (VSMCs), inflammatory cells, and adventitial fibroblasts.
These results suggest that the profile of apoptosis and proliferation after PTCA is regional and cell specific, and attempts to modulate either of these events for therapeutic benefit requires recognition of these differences.</description><subject>Actins - analysis</subject><subject>Angioplasty, Balloon, Coronary - adverse effects</subject><subject>Animals</subject><subject>Antigens - analysis</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Cell Division - physiology</subject><subject>Cell Nucleus - ultrastructure</subject><subject>Coronary Vessels - injuries</subject><subject>Diseases of the cardiovascular system</subject><subject>In Situ Nick-End Labeling</subject><subject>Logistic Models</subject><subject>Medical sciences</subject><subject>Microscopy, Electron</subject><subject>Muscle, Smooth, Vascular - immunology</subject><subject>Muscle, Smooth, Vascular - ultrastructure</subject><subject>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)</subject><subject>Staining and Labeling</subject><subject>Swine</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1LAzEQhoMotVZ_gAdhEfG2NZPPzbEUPwoFQfQc0jSRlO1mTbaH_ntTLD0IA8Mwz8y88yJ0C3gKIOAJw9SGNFXNFEQJLs_QGDhhNeNUnaMxxljVkhJyia5y3pRSUMlHaKSkbCglYzSf9bEfYg65Mt26sq5tqz7FNniXzBBiVxk_uFT1MdnQucrGFDuT9oX-DrFvTR721-jCmza7m2OeoK-X58_5W718f13MZ8vackyH2lLvhCJYGiKBAOGsEW7NV1wSxozgDbOrBjhjgnthV1jaNZFCUi-gMV4BnaDHv71F4M_O5UFvQz4oNp2Lu6yFUoIXWwp4_w_cxF3qijZd7kpCqGQFgj_Ipphzcl73KWzLaxqwPrirMej54kOrRoPQB3fLzN1x8W61devTxNHO0n849k22pvXJdDbkE0YYkRQo_QXpyID6</recordid><startdate>19981020</startdate><enddate>19981020</enddate><creator>MALIK, N</creator><creator>FRANCIS, S. E</creator><creator>HOLT, C. M</creator><creator>GUNN, J</creator><creator>THOMAS, G. L</creator><creator>SHEPHERD, L</creator><creator>CHAMBERLAIN, J</creator><creator>NEWMAN, C. M. H</creator><creator>CUMBERLAND, D. C</creator><creator>CROSSMAN, D. C</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19981020</creationdate><title>Apoptosis and cell proliferation after porcine coronary angioplasty</title><author>MALIK, N ; FRANCIS, S. E ; HOLT, C. M ; GUNN, J ; THOMAS, G. L ; SHEPHERD, L ; CHAMBERLAIN, J ; NEWMAN, C. M. H ; CUMBERLAND, D. C ; CROSSMAN, D. C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-c3fe69207a2712125486ed5b57244a6584cb8154465f6cb07cd27673f618af913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Actins - analysis</topic><topic>Angioplasty, Balloon, Coronary - adverse effects</topic><topic>Animals</topic><topic>Antigens - analysis</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Cell Division - physiology</topic><topic>Cell Nucleus - ultrastructure</topic><topic>Coronary Vessels - injuries</topic><topic>Diseases of the cardiovascular system</topic><topic>In Situ Nick-End Labeling</topic><topic>Logistic Models</topic><topic>Medical sciences</topic><topic>Microscopy, Electron</topic><topic>Muscle, Smooth, Vascular - immunology</topic><topic>Muscle, Smooth, Vascular - ultrastructure</topic><topic>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)</topic><topic>Staining and Labeling</topic><topic>Swine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MALIK, N</creatorcontrib><creatorcontrib>FRANCIS, S. E</creatorcontrib><creatorcontrib>HOLT, C. M</creatorcontrib><creatorcontrib>GUNN, J</creatorcontrib><creatorcontrib>THOMAS, G. L</creatorcontrib><creatorcontrib>SHEPHERD, L</creatorcontrib><creatorcontrib>CHAMBERLAIN, J</creatorcontrib><creatorcontrib>NEWMAN, C. M. H</creatorcontrib><creatorcontrib>CUMBERLAND, D. C</creatorcontrib><creatorcontrib>CROSSMAN, D. C</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MALIK, N</au><au>FRANCIS, S. E</au><au>HOLT, C. M</au><au>GUNN, J</au><au>THOMAS, G. L</au><au>SHEPHERD, L</au><au>CHAMBERLAIN, J</au><au>NEWMAN, C. M. H</au><au>CUMBERLAND, D. C</au><au>CROSSMAN, D. C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptosis and cell proliferation after porcine coronary angioplasty</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1998-10-20</date><risdate>1998</risdate><volume>98</volume><issue>16</issue><spage>1657</spage><epage>1665</epage><pages>1657-1665</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Angioplasty initiates a number of responses in the vessel wall including cellular migration, proliferation, and matrix accumulation, all of which contribute to neointima formation and restenosis. Cellular homeostasis within a tissue depends on the balance between cell proliferation and apoptosis.
Profiles of apoptosis and proliferation were therefore examined in a porcine PTCA injury model over a 28-day period. Forty-two arteries from 21 pigs, harvested at the site of maximal injury at 1, 6, and 18 hours, and 3, 7, 14, and 28 days after PTCA, were examined (n=3 animals per time point). Uninjured arteries were used as controls. Apoptosis was demonstrated by the terminal uridine nick-end labeling (TUNEL) method, transmission electron microscopy (TEM), and DNA fragmentation. Cells traversing the cell cycle were identified by immunostaining for proliferating cell nuclear antigen (PCNA). Apoptosis was not detected in control vessels at all time points nor at 28 days after PTCA. Apoptotic cells were identified at all early time points with a peak at 6 hours (5.1+/-0.26%; compared to uninjured artery, P<0.001) and confirmed by characteristic DNA ladders and TEM findings. Regional analysis showed apoptosis within the media, adventitia, and neointima peaked at 18 hours, 6 hours, and 7 days after PTCA, respectively. In comparison, PCNA staining peaked at 3 days after PTCA (7.16+/-0.29%; compared to 1.78+/-0.08% PCNA-positive cells in the uninjured artery, P<0.001). Profiles of apoptosis and cell proliferation after PTCA were discordant in all layers of the artery except the neointima. These profiles also differed between traumatized and nontraumatized regions of the arterial wall. Immunostaining with cell-type specific markers and TEM analysis revealed that apoptotic cells included vascular smooth muscle cells (VSMCs), inflammatory cells, and adventitial fibroblasts.
These results suggest that the profile of apoptosis and proliferation after PTCA is regional and cell specific, and attempts to modulate either of these events for therapeutic benefit requires recognition of these differences.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9778332</pmid><doi>10.1161/01.cir.98.16.1657</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-7322 |
| ispartof | Circulation (New York, N.Y.), 1998-10, Vol.98 (16), p.1657-1665 |
| issn | 0009-7322 1524-4539 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69965161 |
| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Actins - analysis Angioplasty, Balloon, Coronary - adverse effects Animals Antigens - analysis Apoptosis - physiology Biological and medical sciences Cell Division - physiology Cell Nucleus - ultrastructure Coronary Vessels - injuries Diseases of the cardiovascular system In Situ Nick-End Labeling Logistic Models Medical sciences Microscopy, Electron Muscle, Smooth, Vascular - immunology Muscle, Smooth, Vascular - ultrastructure Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) Staining and Labeling Swine |
| title | Apoptosis and cell proliferation after porcine coronary angioplasty |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-04T11%3A16%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Apoptosis%20and%20cell%20proliferation%20after%20porcine%20coronary%20angioplasty&rft.jtitle=Circulation%20(New%20York,%20N.Y.)&rft.au=MALIK,%20N&rft.date=1998-10-20&rft.volume=98&rft.issue=16&rft.spage=1657&rft.epage=1665&rft.pages=1657-1665&rft.issn=0009-7322&rft.eissn=1524-4539&rft.coden=CIRCAZ&rft_id=info:doi/10.1161/01.cir.98.16.1657&rft_dat=%3Cproquest_cross%3E69965161%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=212722374&rft_id=info:pmid/9778332&rfr_iscdi=true |