Reduced Connexin43 expression limits neointima formation after balloon distension injury in hypercholesterolemic mice
Reducing the expression of the gap junction protein connexin43 (Cx43) inhibits the progression of atherosclerosis, a chronic inflammatory disease. Furthermore, acute vascular injury induced by percutaneous coronary interventions is associated with increased Cx43 expression in neointimal smooth muscl...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2006-06, Vol.113 (24), p.2835-2843 |
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| creator | CHADJICHRISTOS, Christos E MATTER, Christian M ROTH, Isabelle SUTTER, Esther PELLI, Graziano LÜSCHER, Thomas F CHANSON, Marc KWAK, Brenda R |
| description | Reducing the expression of the gap junction protein connexin43 (Cx43) inhibits the progression of atherosclerosis, a chronic inflammatory disease. Furthermore, acute vascular injury induced by percutaneous coronary interventions is associated with increased Cx43 expression in neointimal smooth muscle cells (SMCs). However, the relevance of Cx43 after acute vascular injury remains unclear.
To investigate whether reducing Cx43 expression would affect neointima formation in vivo, we subjected hypercholesterolemic Cx43+/- LDL receptor-deficient (LDLR-/-) mice and Cx43+/+LDLR-/- control littermates to carotid balloon distension injury, which induced marked endothelial denudation and activation of medial SMCs. We observed decreased macrophage infiltration in Cx43+/-LDLR-/- mice 7 days after injury. Similarly, peritoneal macrophages isolated from Cx43+/-LDLR-/- mice showed reduced migration in vitro compared with Cx43+/+LDLR-/- macrophages. Interestingly, Cx43+/-LDLR-/- macrophages also displayed decreased chemotactic activity for SMCs. In addition, we observed less SMC infiltration and proliferation in Cx43+/-LDLR-/- mice 7 and 14 days after balloon angioplasty. Likewise, Cx43+/-LDLR-/- SMCs showed decreased proliferation and migration in vitro compared with Cx43+/+LDLR-/- cells. All these events resulted in a reduction of neointimal thickening after vascular injury in Cx43+/-LDLR-/- mice.
The present study shows for the first time that reducing Cx43 limits neointima formation after acute vascular injury by decreasing the inflammatory response and reducing SMC migration and proliferation. Thus, decreasing Cx43 expression may offer a novel therapeutic strategy for reducing restenosis after percutaneous coronary intervention. |
| doi_str_mv | 10.1161/circulationaha.106.627703 |
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To investigate whether reducing Cx43 expression would affect neointima formation in vivo, we subjected hypercholesterolemic Cx43+/- LDL receptor-deficient (LDLR-/-) mice and Cx43+/+LDLR-/- control littermates to carotid balloon distension injury, which induced marked endothelial denudation and activation of medial SMCs. We observed decreased macrophage infiltration in Cx43+/-LDLR-/- mice 7 days after injury. Similarly, peritoneal macrophages isolated from Cx43+/-LDLR-/- mice showed reduced migration in vitro compared with Cx43+/+LDLR-/- macrophages. Interestingly, Cx43+/-LDLR-/- macrophages also displayed decreased chemotactic activity for SMCs. In addition, we observed less SMC infiltration and proliferation in Cx43+/-LDLR-/- mice 7 and 14 days after balloon angioplasty. Likewise, Cx43+/-LDLR-/- SMCs showed decreased proliferation and migration in vitro compared with Cx43+/+LDLR-/- cells. All these events resulted in a reduction of neointimal thickening after vascular injury in Cx43+/-LDLR-/- mice.
The present study shows for the first time that reducing Cx43 limits neointima formation after acute vascular injury by decreasing the inflammatory response and reducing SMC migration and proliferation. Thus, decreasing Cx43 expression may offer a novel therapeutic strategy for reducing restenosis after percutaneous coronary intervention.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/circulationaha.106.627703</identifier><identifier>PMID: 16769907</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Angioplasty, Balloon - adverse effects ; Animals ; Antihypertensive agents ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiovascular system ; Carotid Artery Diseases - etiology ; Carotid Artery Diseases - therapy ; Carotid Stenosis - etiology ; Carotid Stenosis - prevention & control ; Cell Division ; Cell Movement ; Cells, Cultured - secretion ; Chemotactic Factors - secretion ; Cholesterol - blood ; Connexin 43 - genetics ; Connexin 43 - physiology ; Diet, Atherogenic ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; DNA Replication ; Endothelium, Vascular - pathology ; Human health and pathology ; Hyperlipoproteinemia Type II - blood ; Hyperlipoproteinemia Type II - complications ; Hyperlipoproteinemia Type II - genetics ; Hyperplasia ; Life Sciences ; Macrophages - pathology ; Macrophages - secretion ; Macrophages, Peritoneal - secretion ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular - pathology ; Pharmacology. Drug treatments ; Receptors, LDL - deficiency ; Receptors, LDL - genetics ; Recurrence ; Triglycerides - blood ; Tunica Intima - pathology</subject><ispartof>Circulation (New York, N.Y.), 2006-06, Vol.113 (24), p.2835-2843</ispartof><rights>2006 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-265d0d23cb19400427ad499c3b9211438e158c44d323dbbaa8e30d03024cda973</citedby><cites>FETCH-LOGICAL-c488t-265d0d23cb19400427ad499c3b9211438e158c44d323dbbaa8e30d03024cda973</cites><orcidid>0000-0001-6657-7900</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3685,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17930483$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16769907$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03838485$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>CHADJICHRISTOS, Christos E</creatorcontrib><creatorcontrib>MATTER, Christian M</creatorcontrib><creatorcontrib>ROTH, Isabelle</creatorcontrib><creatorcontrib>SUTTER, Esther</creatorcontrib><creatorcontrib>PELLI, Graziano</creatorcontrib><creatorcontrib>LÜSCHER, Thomas F</creatorcontrib><creatorcontrib>CHANSON, Marc</creatorcontrib><creatorcontrib>KWAK, Brenda R</creatorcontrib><title>Reduced Connexin43 expression limits neointima formation after balloon distension injury in hypercholesterolemic mice</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Reducing the expression of the gap junction protein connexin43 (Cx43) inhibits the progression of atherosclerosis, a chronic inflammatory disease. Furthermore, acute vascular injury induced by percutaneous coronary interventions is associated with increased Cx43 expression in neointimal smooth muscle cells (SMCs). However, the relevance of Cx43 after acute vascular injury remains unclear.
To investigate whether reducing Cx43 expression would affect neointima formation in vivo, we subjected hypercholesterolemic Cx43+/- LDL receptor-deficient (LDLR-/-) mice and Cx43+/+LDLR-/- control littermates to carotid balloon distension injury, which induced marked endothelial denudation and activation of medial SMCs. We observed decreased macrophage infiltration in Cx43+/-LDLR-/- mice 7 days after injury. Similarly, peritoneal macrophages isolated from Cx43+/-LDLR-/- mice showed reduced migration in vitro compared with Cx43+/+LDLR-/- macrophages. Interestingly, Cx43+/-LDLR-/- macrophages also displayed decreased chemotactic activity for SMCs. In addition, we observed less SMC infiltration and proliferation in Cx43+/-LDLR-/- mice 7 and 14 days after balloon angioplasty. Likewise, Cx43+/-LDLR-/- SMCs showed decreased proliferation and migration in vitro compared with Cx43+/+LDLR-/- cells. All these events resulted in a reduction of neointimal thickening after vascular injury in Cx43+/-LDLR-/- mice.
The present study shows for the first time that reducing Cx43 limits neointima formation after acute vascular injury by decreasing the inflammatory response and reducing SMC migration and proliferation. Thus, decreasing Cx43 expression may offer a novel therapeutic strategy for reducing restenosis after percutaneous coronary intervention.</description><subject>Angioplasty, Balloon - adverse effects</subject><subject>Animals</subject><subject>Antihypertensive agents</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular system</subject><subject>Carotid Artery Diseases - etiology</subject><subject>Carotid Artery Diseases - therapy</subject><subject>Carotid Stenosis - etiology</subject><subject>Carotid Stenosis - prevention & control</subject><subject>Cell Division</subject><subject>Cell Movement</subject><subject>Cells, Cultured - secretion</subject><subject>Chemotactic Factors - secretion</subject><subject>Cholesterol - blood</subject><subject>Connexin 43 - genetics</subject><subject>Connexin 43 - physiology</subject><subject>Diet, Atherogenic</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>DNA Replication</subject><subject>Endothelium, Vascular - pathology</subject><subject>Human health and pathology</subject><subject>Hyperlipoproteinemia Type II - blood</subject><subject>Hyperlipoproteinemia Type II - complications</subject><subject>Hyperlipoproteinemia Type II - genetics</subject><subject>Hyperplasia</subject><subject>Life Sciences</subject><subject>Macrophages - pathology</subject><subject>Macrophages - secretion</subject><subject>Macrophages, Peritoneal - secretion</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptors, LDL - deficiency</subject><subject>Receptors, LDL - genetics</subject><subject>Recurrence</subject><subject>Triglycerides - blood</subject><subject>Tunica Intima - pathology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkV1r2zAUhsXYWLNuf2F4Fxv0wpm-rI9LY7YmEFYo7bWQJZmoyHIm2aX591OasF6Iwzl63vPBC8A3BNcIMfTT-GSWoGc_Rb3XawTZmmHOIXkHVqjBtKYNke_BCkIoa04wvgKfcn4qKSO8-QiuEONMSshXYLl3djHOVt0Uo3vxkZLKvRySy7l0r4If_Zyr6CYfZz_qapjS-Dq40sPsUtXrEKaSWZ9nF181Pj4t6VhCtT8eXDL7KbjymUoYvanKc5_Bh0GH7L5c4jV4_P3rodvUu7vbbdfuakOFmGvMGgstJqZHkkJIMdeWSmlILzFClAiHGmEotQQT2_daC0eghQRiaqyWnFyDm3PfvQ7qkMoB6agm7dWm3alTDRJBBBXNMyrsjzN7SNPfpWysRp-NC0GX65esmICyYfAEyjNo0pRzcsP_zgiqkz-q2953j7v2YXv3p920pczU2Z-i_XoZsvSjs2_KiyEF-H4BdDY6DElH4_MbxyWBVBDyDx80naE</recordid><startdate>20060620</startdate><enddate>20060620</enddate><creator>CHADJICHRISTOS, Christos E</creator><creator>MATTER, Christian M</creator><creator>ROTH, Isabelle</creator><creator>SUTTER, Esther</creator><creator>PELLI, Graziano</creator><creator>LÜSCHER, Thomas F</creator><creator>CHANSON, Marc</creator><creator>KWAK, Brenda R</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association</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>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-6657-7900</orcidid></search><sort><creationdate>20060620</creationdate><title>Reduced Connexin43 expression limits neointima formation after balloon distension injury in hypercholesterolemic mice</title><author>CHADJICHRISTOS, Christos E ; MATTER, Christian M ; ROTH, Isabelle ; SUTTER, Esther ; PELLI, Graziano ; LÜSCHER, Thomas F ; CHANSON, Marc ; KWAK, Brenda R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-265d0d23cb19400427ad499c3b9211438e158c44d323dbbaa8e30d03024cda973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Angioplasty, Balloon - adverse effects</topic><topic>Animals</topic><topic>Antihypertensive agents</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular system</topic><topic>Carotid Artery Diseases - etiology</topic><topic>Carotid Artery Diseases - therapy</topic><topic>Carotid Stenosis - etiology</topic><topic>Carotid Stenosis - prevention & control</topic><topic>Cell Division</topic><topic>Cell Movement</topic><topic>Cells, Cultured - secretion</topic><topic>Chemotactic Factors - secretion</topic><topic>Cholesterol - blood</topic><topic>Connexin 43 - genetics</topic><topic>Connexin 43 - physiology</topic><topic>Diet, Atherogenic</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>DNA Replication</topic><topic>Endothelium, Vascular - pathology</topic><topic>Human health and pathology</topic><topic>Hyperlipoproteinemia Type II - blood</topic><topic>Hyperlipoproteinemia Type II - complications</topic><topic>Hyperlipoproteinemia Type II - genetics</topic><topic>Hyperplasia</topic><topic>Life Sciences</topic><topic>Macrophages - pathology</topic><topic>Macrophages - secretion</topic><topic>Macrophages, Peritoneal - secretion</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptors, LDL - deficiency</topic><topic>Receptors, LDL - genetics</topic><topic>Recurrence</topic><topic>Triglycerides - blood</topic><topic>Tunica Intima - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHADJICHRISTOS, Christos E</creatorcontrib><creatorcontrib>MATTER, Christian M</creatorcontrib><creatorcontrib>ROTH, Isabelle</creatorcontrib><creatorcontrib>SUTTER, Esther</creatorcontrib><creatorcontrib>PELLI, Graziano</creatorcontrib><creatorcontrib>LÜSCHER, Thomas F</creatorcontrib><creatorcontrib>CHANSON, Marc</creatorcontrib><creatorcontrib>KWAK, Brenda R</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>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHADJICHRISTOS, Christos E</au><au>MATTER, Christian M</au><au>ROTH, Isabelle</au><au>SUTTER, Esther</au><au>PELLI, Graziano</au><au>LÜSCHER, Thomas F</au><au>CHANSON, Marc</au><au>KWAK, Brenda R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced Connexin43 expression limits neointima formation after balloon distension injury in hypercholesterolemic mice</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2006-06-20</date><risdate>2006</risdate><volume>113</volume><issue>24</issue><spage>2835</spage><epage>2843</epage><pages>2835-2843</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Reducing the expression of the gap junction protein connexin43 (Cx43) inhibits the progression of atherosclerosis, a chronic inflammatory disease. Furthermore, acute vascular injury induced by percutaneous coronary interventions is associated with increased Cx43 expression in neointimal smooth muscle cells (SMCs). However, the relevance of Cx43 after acute vascular injury remains unclear.
To investigate whether reducing Cx43 expression would affect neointima formation in vivo, we subjected hypercholesterolemic Cx43+/- LDL receptor-deficient (LDLR-/-) mice and Cx43+/+LDLR-/- control littermates to carotid balloon distension injury, which induced marked endothelial denudation and activation of medial SMCs. We observed decreased macrophage infiltration in Cx43+/-LDLR-/- mice 7 days after injury. Similarly, peritoneal macrophages isolated from Cx43+/-LDLR-/- mice showed reduced migration in vitro compared with Cx43+/+LDLR-/- macrophages. Interestingly, Cx43+/-LDLR-/- macrophages also displayed decreased chemotactic activity for SMCs. In addition, we observed less SMC infiltration and proliferation in Cx43+/-LDLR-/- mice 7 and 14 days after balloon angioplasty. Likewise, Cx43+/-LDLR-/- SMCs showed decreased proliferation and migration in vitro compared with Cx43+/+LDLR-/- cells. All these events resulted in a reduction of neointimal thickening after vascular injury in Cx43+/-LDLR-/- mice.
The present study shows for the first time that reducing Cx43 limits neointima formation after acute vascular injury by decreasing the inflammatory response and reducing SMC migration and proliferation. Thus, decreasing Cx43 expression may offer a novel therapeutic strategy for reducing restenosis after percutaneous coronary intervention.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>16769907</pmid><doi>10.1161/circulationaha.106.627703</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-6657-7900</orcidid></addata></record> |
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| subjects | Angioplasty, Balloon - adverse effects Animals Antihypertensive agents Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular system Carotid Artery Diseases - etiology Carotid Artery Diseases - therapy Carotid Stenosis - etiology Carotid Stenosis - prevention & control Cell Division Cell Movement Cells, Cultured - secretion Chemotactic Factors - secretion Cholesterol - blood Connexin 43 - genetics Connexin 43 - physiology Diet, Atherogenic Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous DNA Replication Endothelium, Vascular - pathology Human health and pathology Hyperlipoproteinemia Type II - blood Hyperlipoproteinemia Type II - complications Hyperlipoproteinemia Type II - genetics Hyperplasia Life Sciences Macrophages - pathology Macrophages - secretion Macrophages, Peritoneal - secretion Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Muscle, Smooth, Vascular - pathology Pharmacology. Drug treatments Receptors, LDL - deficiency Receptors, LDL - genetics Recurrence Triglycerides - blood Tunica Intima - pathology |
| title | Reduced Connexin43 expression limits neointima formation after balloon distension injury in hypercholesterolemic mice |
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