{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:50072"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:50072","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Der Einfluss von N-Cadherin auf die Migration glatter Gefäßmuskelzellen im Rahmen der Restenoseentstehung","abstract":"Objective: In this study we analyze the role of N-cadherin during human arterial smooth muscle cell (haSMC) migration and Rho-family GTPases-mediated dynamic rearrangement of cell–cell adhesion. Methods: Expression patterns of N-cadherin and beta-catenin were analyzed in vivo using a domestic pig restenosis model (expression after 14, 28, and 90 days) as well as in vitro by analysis of quiescent and migratory haSMCs. Upregulation of N-cadherin expression was induced by transient sense transfection whereas expression was downregulated by antisense transfection. For functional inhibition, antibody GC-4 was used. Quantification of cell migration was detected by Boyden chamber assays. Regulation of RhoA GTPase was tested by assessment of RhoA activity. Results: The analysis of N-cadherin expression in vivo by a porcine restenosis model revealed downregulation in the neointima after 14 days. After 28 days, N-cadherin expression was slightly restored, while after 90 days, no difference between medial and neointimal expression was detectable. During the whole period beta-catenin levels remained unchanged. According to these results the analysis in vitro showed a significant downregulation of N-cadherin in migratory haSMCs compared to quiescent cells. Overexpression of N-cadherin after transfection leaded to reduction of haSMC migration by 87% (P<0.001). By contrast, inhibition of N-cadherin in quiescent haSMCs by GC-4 increased the migratory potential by 87% (P<0.01). After N-cadherin overexpression in haSMCs RhoA activity was significantly upregulated while RhoA activity was blocked by GC-4. Conclusions: These results indicate that the regulation of haSMC attachment by N-cadherins is essential for haSMC migration. Modification of N-cadherin expression and activity induces RhoA signaling with relevance for the reorganization of the actin cytoskeleton.","abstract_html":"Objective: In this study we analyze the role of N-cadherin during human arterial smooth muscle cell (haSMC) migration and Rho-family GTPases-mediated dynamic rearrangement of cell–cell adhesion. Methods: Expression patterns of N-cadherin and beta-catenin were analyzed in vivo using a domestic pig restenosis model (expression after 14, 28, and 90 days) as well as in vitro by analysis of quiescent and migratory haSMCs. Upregulation of N-cadherin expression was induced by transient sense transfection whereas expression was downregulated by antisense transfection. For functional inhibition, antibody GC-4 was used. Quantification of cell migration was detected by Boyden chamber assays. Regulation of RhoA GTPase was tested by assessment of RhoA activity. Results: The analysis of N-cadherin expression in vivo by a porcine restenosis model revealed downregulation in the neointima after 14 days. After 28 days, N-cadherin expression was slightly restored, while after 90 days, no difference between medial and neointimal expression was detectable. During the whole period beta-catenin levels remained unchanged. According to these results the analysis in vitro showed a significant downregulation of N-cadherin in migratory haSMCs compared to quiescent cells. Overexpression of N-cadherin after transfection leaded to reduction of haSMC migration by 87% (P&lt;0.001). By contrast, inhibition of N-cadherin in quiescent haSMCs by GC-4 increased the migratory potential by 87% (P&lt;0.01). After N-cadherin overexpression in haSMCs RhoA activity was significantly upregulated while RhoA activity was blocked by GC-4. Conclusions: These results indicate that the regulation of haSMC attachment by N-cadherins is essential for haSMC migration. Modification of N-cadherin expression and activity induces RhoA signaling with relevance for the reorganization of the actin cytoskeleton.","abstract_has_math":false,"creators":["Stein, Julia"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Blindt, Rüdiger"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2008,"date_issued":"2008","date_published":"2008","updated_at":"2026-07-30T19:40:16Z","subjects":["info:eu-repo/classification/ddc/610","Adhäsionsproteine","Restenose","Gefäßmuskelzelle","Medizin","Adhesion molecules","Restenosis","Smooth muscle cells"],"languages":["ger"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112634%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112634%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112634%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/50072","outbound_label":"Repository record","outbound_source":"dc:identifier"},"source_record":{"url":"https://publications.rwth-aachen.de/oai2d?verb=GetRecord&metadataPrefix=oai_dc&identifier=oai%3Apublications.rwth-aachen.de%3A50072","prefix":"oai_dc"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Blindt, Rüdiger"]},{"key":"dc:creator","label":"Author","values":["Stein, Julia"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2008"]},{"key":"dc:publisher","label":"Institution","values":["Publikationsserver der RWTH Aachen University"]},{"key":"dc:relation","label":"Dc Relation","values":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-22209"]},{"key":"dc:type","label":"Dc Type","values":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["info:eu-repo/classification/ddc/610","Adhäsionsproteine","Restenose","Gefäßmuskelzelle","Medizin","Adhesion molecules","Restenosis","Smooth muscle cells"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["ger"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/record/50072","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112634%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Objective: In this study we analyze the role of N-cadherin during human arterial smooth muscle cell (haSMC) migration and Rho-family GTPases-mediated dynamic rearrangement of cell–cell adhesion. Methods: Expression patterns of N-cadherin and beta-catenin were analyzed in vivo using a domestic pig restenosis model (expression after 14, 28, and 90 days) as well as in vitro by analysis of quiescent and migratory haSMCs. Upregulation of N-cadherin expression was induced by transient sense transfection whereas expression was downregulated by antisense transfection. For functional inhibition, antibody GC-4 was used. Quantification of cell migration was detected by Boyden chamber assays. Regulation of RhoA GTPase was tested by assessment of RhoA activity. Results: The analysis of N-cadherin expression in vivo by a porcine restenosis model revealed downregulation in the neointima after 14 days. After 28 days, N-cadherin expression was slightly restored, while after 90 days, no difference between medial and neointimal expression was detectable. During the whole period beta-catenin levels remained unchanged. According to these results the analysis in vitro showed a significant downregulation of N-cadherin in migratory haSMCs compared to quiescent cells. Overexpression of N-cadherin after transfection leaded to reduction of haSMC migration by 87% (P<0.001). By contrast, inhibition of N-cadherin in quiescent haSMCs by GC-4 increased the migratory potential by 87% (P<0.01). After N-cadherin overexpression in haSMCs RhoA activity was significantly upregulated while RhoA activity was blocked by GC-4. Conclusions: These results indicate that the regulation of haSMC attachment by N-cadherins is essential for haSMC migration. Modification of N-cadherin expression and activity induces RhoA signaling with relevance for the reorganization of the actin cytoskeleton."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University 67 S. : Ill., graph. Darst. (2008). = Aachen, Techn. Hochsch., Diss., 2008"]},{"key":"dc:title","label":"Title","values":["Der Einfluss von N-Cadherin auf die Migration glatter Gefäßmuskelzellen im Rahmen der Restenoseentstehung"]}]}],"canonical_facts":{"dc:contributor":["Blindt, Rüdiger"],"dc:coverage":["DE"],"dc:creator":["Stein, Julia"],"dc:date":["2008"],"dc:description":["Objective: In this study we analyze the role of N-cadherin during human arterial smooth muscle cell (haSMC) migration and Rho-family GTPases-mediated dynamic rearrangement of cell–cell adhesion. Methods: Expression patterns of N-cadherin and beta-catenin were analyzed in vivo using a domestic pig restenosis model (expression after 14, 28, and 90 days) as well as in vitro by analysis of quiescent and migratory haSMCs. Upregulation of N-cadherin expression was induced by transient sense transfection whereas expression was downregulated by antisense transfection. For functional inhibition, antibody GC-4 was used. Quantification of cell migration was detected by Boyden chamber assays. Regulation of RhoA GTPase was tested by assessment of RhoA activity. Results: The analysis of N-cadherin expression in vivo by a porcine restenosis model revealed downregulation in the neointima after 14 days. After 28 days, N-cadherin expression was slightly restored, while after 90 days, no difference between medial and neointimal expression was detectable. During the whole period beta-catenin levels remained unchanged. According to these results the analysis in vitro showed a significant downregulation of N-cadherin in migratory haSMCs compared to quiescent cells. Overexpression of N-cadherin after transfection leaded to reduction of haSMC migration by 87% (P<0.001). By contrast, inhibition of N-cadherin in quiescent haSMCs by GC-4 increased the migratory potential by 87% (P<0.01). After N-cadherin overexpression in haSMCs RhoA activity was significantly upregulated while RhoA activity was blocked by GC-4. Conclusions: These results indicate that the regulation of haSMC attachment by N-cadherins is essential for haSMC migration. Modification of N-cadherin expression and activity induces RhoA signaling with relevance for the reorganization of the actin cytoskeleton."],"dc:identifier":["https://publications.rwth-aachen.de/record/50072","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112634%22"],"dc:language":["ger"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-22209"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University 67 S. : Ill., graph. Darst. (2008). = Aachen, Techn. Hochsch., Diss., 2008"],"dc:subject":["info:eu-repo/classification/ddc/610","Adhäsionsproteine","Restenose","Gefäßmuskelzelle","Medizin","Adhesion molecules","Restenosis","Smooth muscle cells"],"dc:title":["Der Einfluss von N-Cadherin auf die Migration glatter Gefäßmuskelzellen im Rahmen der Restenoseentstehung"],"dc:type":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]},"updated_at":"2026-07-30T19:40:16Z"}