Biomechanically Induced Gene iex-1 Inhibits Vascular Smooth Muscle Cell Proliferation and Neointima Formation

ABSTRACT—Mechanotransduction plays a prominent role in vascular pathophysiology but is incompletely understood. In this study, we report the biomechanical induction of the immediate early response gene iex-1 in vascular smooth muscle cells (SMCs). Mechanical induction of iex-1 was confirmed by North...

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Published in:Circulation research 2003-12, Vol.93 (12), p.1210-1217
Main Authors: Schulze, P Christian, de Keulenaer, Gilles W, Kassik, Kimberly A, Takahashi, Tomosaburo, Chen, Zhiping, Simon, Daniel I, Lee, Richard T
Format: Article
Language:English
Subjects:
Animals
Apolipoproteins E - genetics
Apoptosis Regulatory Proteins
Arteriosclerosis - genetics
Arteriosclerosis - physiopathology
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Carotid Artery Injuries - genetics
Carotid Artery Injuries - physiopathology
Cell Cycle - physiology
Cell Division - physiology
Cells, Cultured
Gene Expression Regulation
Green Fluorescent Proteins
Humans
Immediate-Early Proteins - genetics
Immediate-Early Proteins - metabolism
Luminescent Proteins - genetics
Luminescent Proteins - metabolism
Mechanotransduction, Cellular - physiology
Medical sciences
Membrane Proteins
Mice
Mice, Knockout
Muscle, Smooth, Vascular - cytology
Muscle, Smooth, Vascular - metabolism
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
NF-kappa B - metabolism
Receptors, LDL - genetics
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Stress, Mechanical
Tunica Intima - physiopathology
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Lee, Richard T
description ABSTRACT—Mechanotransduction plays a prominent role in vascular pathophysiology but is incompletely understood. In this study, we report the biomechanical induction of the immediate early response gene iex-1 in vascular smooth muscle cells (SMCs). Mechanical induction of iex-1 was confirmed by Northern (30-fold induction after 2 hours) and Western (6-fold induction after 24 hours) analyses. Expression of iex-1 was regulated by mechanical activation of nuclear factor (NF)-κB and abolished by overexpression of IκB in SMCs. The function of iex-1 in SMCs was explored by gene transfer using adenoviral vectors overexpressing iex-1. After 48 hours of 4% cyclic mechanical strain, adenoviral vectors overexpressing iex-1–infected cells had lower [H]-thymidine incorporation compared with AdGFP-infected controls (71.3±8.5% versus 180.2±19.4% in controls; P
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In this study, we report the biomechanical induction of the immediate early response gene iex-1 in vascular smooth muscle cells (SMCs). Mechanical induction of iex-1 was confirmed by Northern (30-fold induction after 2 hours) and Western (6-fold induction after 24 hours) analyses. Expression of iex-1 was regulated by mechanical activation of nuclear factor (NF)-κB and abolished by overexpression of IκB in SMCs. The function of iex-1 in SMCs was explored by gene transfer using adenoviral vectors overexpressing iex-1. After 48 hours of 4% cyclic mechanical strain, adenoviral vectors overexpressing iex-1–infected cells had lower [H]-thymidine incorporation compared with AdGFP-infected controls (71.3±8.5% versus 180.2±19.4% in controls; P &lt;0.001). Overexpression of iex-1 suppressed mitogenesis induced by platelet-derived growth factor (208.1±108.3% versus 290.0±120.5% in controls; P &lt;0.05). This was accompanied by reduced degradation of p27, inhibition of Rb hyperphosphorylation, and reduced cell cycle progression. To investigate functional effects of iex-1 in vivo, we performed carotid artery mechanical injury and endothelial denudation in low-density lipoprotein receptor–deficient mice followed by intraluminal injection of adenoviral vectors (3×10 pfu in 50 μL) for overexpression of iex-1 or gfp (control). Vascular overexpression of iex-1 reduced neointima formation 2 weeks after injury (intima/media ratio, 0.23±0.04 versus 0.5±0.24 in controls; P &lt;0.05). Our findings demonstrate that biomechanical strain induces iex-1 with subsequent antiproliferative effects in SMCs and that selective gene transfer of iex-1 inhibits the local vascular response after injury. These findings suggest that the induction of iex-1 represents a novel negative biomechanical feedback mechanism limiting the vascular response to injury.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000103635.38096.2F</identifier><identifier>PMID: 14592999</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Apolipoproteins E - genetics ; Apoptosis Regulatory Proteins ; Arteriosclerosis - genetics ; Arteriosclerosis - physiopathology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Carotid Artery Injuries - genetics ; Carotid Artery Injuries - physiopathology ; Cell Cycle - physiology ; Cell Division - physiology ; Cells, Cultured ; Gene Expression Regulation ; Green Fluorescent Proteins ; Humans ; Immediate-Early Proteins - genetics ; Immediate-Early Proteins - metabolism ; Luminescent Proteins - genetics ; Luminescent Proteins - metabolism ; Mechanotransduction, Cellular - physiology ; Medical sciences ; Membrane Proteins ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; NF-kappa B - metabolism ; Receptors, LDL - genetics ; Recombinant Fusion Proteins - genetics ; Recombinant Fusion Proteins - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Stress, Mechanical ; Tunica Intima - physiopathology</subject><ispartof>Circulation research, 2003-12, Vol.93 (12), p.1210-1217</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Dec 12 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5070-39196f45529ef7870777c649a9480158a234c93b9cee857b365b5ca7c965f3143</citedby><cites>FETCH-LOGICAL-c5070-39196f45529ef7870777c649a9480158a234c93b9cee857b365b5ca7c965f3143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=15367504$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14592999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schulze, P Christian</creatorcontrib><creatorcontrib>de Keulenaer, Gilles W</creatorcontrib><creatorcontrib>Kassik, Kimberly A</creatorcontrib><creatorcontrib>Takahashi, Tomosaburo</creatorcontrib><creatorcontrib>Chen, Zhiping</creatorcontrib><creatorcontrib>Simon, Daniel I</creatorcontrib><creatorcontrib>Lee, Richard T</creatorcontrib><title>Biomechanically Induced Gene iex-1 Inhibits Vascular Smooth Muscle Cell Proliferation and Neointima Formation</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>ABSTRACT—Mechanotransduction plays a prominent role in vascular pathophysiology but is incompletely understood. In this study, we report the biomechanical induction of the immediate early response gene iex-1 in vascular smooth muscle cells (SMCs). Mechanical induction of iex-1 was confirmed by Northern (30-fold induction after 2 hours) and Western (6-fold induction after 24 hours) analyses. Expression of iex-1 was regulated by mechanical activation of nuclear factor (NF)-κB and abolished by overexpression of IκB in SMCs. The function of iex-1 in SMCs was explored by gene transfer using adenoviral vectors overexpressing iex-1. After 48 hours of 4% cyclic mechanical strain, adenoviral vectors overexpressing iex-1–infected cells had lower [H]-thymidine incorporation compared with AdGFP-infected controls (71.3±8.5% versus 180.2±19.4% in controls; P &lt;0.001). Overexpression of iex-1 suppressed mitogenesis induced by platelet-derived growth factor (208.1±108.3% versus 290.0±120.5% in controls; P &lt;0.05). This was accompanied by reduced degradation of p27, inhibition of Rb hyperphosphorylation, and reduced cell cycle progression. To investigate functional effects of iex-1 in vivo, we performed carotid artery mechanical injury and endothelial denudation in low-density lipoprotein receptor–deficient mice followed by intraluminal injection of adenoviral vectors (3×10 pfu in 50 μL) for overexpression of iex-1 or gfp (control). Vascular overexpression of iex-1 reduced neointima formation 2 weeks after injury (intima/media ratio, 0.23±0.04 versus 0.5±0.24 in controls; P &lt;0.05). Our findings demonstrate that biomechanical strain induces iex-1 with subsequent antiproliferative effects in SMCs and that selective gene transfer of iex-1 inhibits the local vascular response after injury. 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Vascular system</subject><subject>Carotid Artery Injuries - genetics</subject><subject>Carotid Artery Injuries - physiopathology</subject><subject>Cell Cycle - physiology</subject><subject>Cell Division - physiology</subject><subject>Cells, Cultured</subject><subject>Gene Expression Regulation</subject><subject>Green Fluorescent Proteins</subject><subject>Humans</subject><subject>Immediate-Early Proteins - genetics</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Luminescent Proteins - genetics</subject><subject>Luminescent Proteins - metabolism</subject><subject>Mechanotransduction, Cellular - physiology</subject><subject>Medical sciences</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Receptors, LDL - genetics</subject><subject>Recombinant Fusion Proteins - genetics</subject><subject>Recombinant Fusion Proteins - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Stress, Mechanical</subject><subject>Tunica Intima - physiopathology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNpdkVtv1DAQhS0EotvCX0BWJXhL8DWOeYNVt1QqF1Hg1XK8E8XFiYudqPTf191daSX8MtLoG885cxA6p6SmtKHvCa1_XNzUpDxKeMNlzVuim5ptnqEVlUxUQir6HK0KoCvFOTlBpznfFlxwpl-iEyqkZlrrFRo_-TiCG-zknQ3hAV9N28XBFl_CBNjDv4qW1uA7P2f822a3BJvwzRjjPOAvS3YB8BpCwN9TDL6HZGcfJ2ynLf4K0U-zHy3exDTu-q_Qi96GDK8P9Qz92lz8XH-urr9dXq0_XldOEkUqrqlueiEl09CrVhGllGuEtlq0hMrWMi6c5p12AK1UHW9kJ51VTjey58XkGXq3__cuxb8L5NmMPrsi004Ql2wUFYrIRhfw_D_wNi5pKtoMo0wIxgQp0Ic95FLMOUFv7lKxlR4MJeYpEUOoKYmYYyJml4hhmzL85rBh6UbYHkcPERTg7QEo17WhT3ZyPh85yRslyZMnsefuY5gh5T9huYdkBrBhHnarOaGsYqXSop1UezGPt86iWg</recordid><startdate>20031212</startdate><enddate>20031212</enddate><creator>Schulze, P Christian</creator><creator>de Keulenaer, Gilles W</creator><creator>Kassik, Kimberly A</creator><creator>Takahashi, Tomosaburo</creator><creator>Chen, Zhiping</creator><creator>Simon, Daniel I</creator><creator>Lee, Richard T</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams &amp; Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20031212</creationdate><title>Biomechanically Induced Gene iex-1 Inhibits Vascular Smooth Muscle Cell Proliferation and Neointima Formation</title><author>Schulze, P Christian ; de Keulenaer, Gilles W ; Kassik, Kimberly A ; Takahashi, Tomosaburo ; Chen, Zhiping ; Simon, Daniel I ; Lee, Richard T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5070-39196f45529ef7870777c649a9480158a234c93b9cee857b365b5ca7c965f3143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apolipoproteins E - genetics</topic><topic>Apoptosis Regulatory Proteins</topic><topic>Arteriosclerosis - genetics</topic><topic>Arteriosclerosis - physiopathology</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>Carotid Artery Injuries - genetics</topic><topic>Carotid Artery Injuries - physiopathology</topic><topic>Cell Cycle - physiology</topic><topic>Cell Division - physiology</topic><topic>Cells, Cultured</topic><topic>Gene Expression Regulation</topic><topic>Green Fluorescent Proteins</topic><topic>Humans</topic><topic>Immediate-Early Proteins - genetics</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Luminescent Proteins - genetics</topic><topic>Luminescent Proteins - metabolism</topic><topic>Mechanotransduction, Cellular - physiology</topic><topic>Medical sciences</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Receptors, LDL - genetics</topic><topic>Recombinant Fusion Proteins - genetics</topic><topic>Recombinant Fusion Proteins - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Stress, Mechanical</topic><topic>Tunica Intima - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schulze, P Christian</creatorcontrib><creatorcontrib>de Keulenaer, Gilles W</creatorcontrib><creatorcontrib>Kassik, Kimberly A</creatorcontrib><creatorcontrib>Takahashi, Tomosaburo</creatorcontrib><creatorcontrib>Chen, Zhiping</creatorcontrib><creatorcontrib>Simon, Daniel I</creatorcontrib><creatorcontrib>Lee, Richard T</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>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schulze, P Christian</au><au>de Keulenaer, Gilles W</au><au>Kassik, Kimberly A</au><au>Takahashi, Tomosaburo</au><au>Chen, Zhiping</au><au>Simon, Daniel I</au><au>Lee, Richard T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biomechanically Induced Gene iex-1 Inhibits Vascular Smooth Muscle Cell Proliferation and Neointima Formation</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2003-12-12</date><risdate>2003</risdate><volume>93</volume><issue>12</issue><spage>1210</spage><epage>1217</epage><pages>1210-1217</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACT—Mechanotransduction plays a prominent role in vascular pathophysiology but is incompletely understood. In this study, we report the biomechanical induction of the immediate early response gene iex-1 in vascular smooth muscle cells (SMCs). Mechanical induction of iex-1 was confirmed by Northern (30-fold induction after 2 hours) and Western (6-fold induction after 24 hours) analyses. Expression of iex-1 was regulated by mechanical activation of nuclear factor (NF)-κB and abolished by overexpression of IκB in SMCs. The function of iex-1 in SMCs was explored by gene transfer using adenoviral vectors overexpressing iex-1. After 48 hours of 4% cyclic mechanical strain, adenoviral vectors overexpressing iex-1–infected cells had lower [H]-thymidine incorporation compared with AdGFP-infected controls (71.3±8.5% versus 180.2±19.4% in controls; P &lt;0.001). Overexpression of iex-1 suppressed mitogenesis induced by platelet-derived growth factor (208.1±108.3% versus 290.0±120.5% in controls; P &lt;0.05). This was accompanied by reduced degradation of p27, inhibition of Rb hyperphosphorylation, and reduced cell cycle progression. To investigate functional effects of iex-1 in vivo, we performed carotid artery mechanical injury and endothelial denudation in low-density lipoprotein receptor–deficient mice followed by intraluminal injection of adenoviral vectors (3×10 pfu in 50 μL) for overexpression of iex-1 or gfp (control). Vascular overexpression of iex-1 reduced neointima formation 2 weeks after injury (intima/media ratio, 0.23±0.04 versus 0.5±0.24 in controls; P &lt;0.05). Our findings demonstrate that biomechanical strain induces iex-1 with subsequent antiproliferative effects in SMCs and that selective gene transfer of iex-1 inhibits the local vascular response after injury. These findings suggest that the induction of iex-1 represents a novel negative biomechanical feedback mechanism limiting the vascular response to injury.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>14592999</pmid><doi>10.1161/01.RES.0000103635.38096.2F</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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source Freely Accessible Journals
subjects Animals
Apolipoproteins E - genetics
Apoptosis Regulatory Proteins
Arteriosclerosis - genetics
Arteriosclerosis - physiopathology
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Carotid Artery Injuries - genetics
Carotid Artery Injuries - physiopathology
Cell Cycle - physiology
Cell Division - physiology
Cells, Cultured
Gene Expression Regulation
Green Fluorescent Proteins
Humans
Immediate-Early Proteins - genetics
Immediate-Early Proteins - metabolism
Luminescent Proteins - genetics
Luminescent Proteins - metabolism
Mechanotransduction, Cellular - physiology
Medical sciences
Membrane Proteins
Mice
Mice, Knockout
Muscle, Smooth, Vascular - cytology
Muscle, Smooth, Vascular - metabolism
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
NF-kappa B - metabolism
Receptors, LDL - genetics
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Stress, Mechanical
Tunica Intima - physiopathology
title Biomechanically Induced Gene iex-1 Inhibits Vascular Smooth Muscle Cell Proliferation and Neointima Formation
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