Connexin43 Inhibition Prevents Human Vein Grafts Intimal Hyperplasia

Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia (IH). Intercellular communication mediated by Connexins (Cx) regulates differentiation, growth and proliferation in various cell types. Microar...

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Published inPloS one Vol. 10; no. 9; p. e0138847
Main Authors Longchamp, Alban, Allagnat, Florent, Alonso, Florian, Kuppler, Christopher, Dubuis, Céline, Ozaki, Charles-Keith, Mitchell, James R, Berceli, Scott, Corpataux, Jean-Marc, Déglise, Sébastien, Haefliger, Jacques-Antoine
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 23.09.2015
Public Library of Science (PLoS)
Subjects
Analysis
Animals
Arteriosclerosis
Atherosclerosis
Biology
Carotid arteries
Cell Proliferation
Cell signaling
Connexin 43
Connexin 43 - antagonists & inhibitors
Connexin 43 - physiology
Connexins
DNA microarrays
Genetic aspects
Grafting
Grafts
Hemodynamics
Humans
Hyperplasia
Hyperplasia - prevention & control
Implantation
Jugular vein
Laboratories
Male
Medicine
Membrane proteins
Muscle, Smooth, Vascular - pathology
Muscles
Perfusion
Physiological aspects
Physiology
Prevention
Public health
Rabbits
Ribonucleic acid
Risk factors
RNA
RNA-mediated interference
Shear stress
Smooth muscle
Thrombosis
Tunica Intima - pathology
Vascular Grafting
Vascular surgery
Veins
Veins & arteries
Veins - transplantation
Womens health
United States
Florida
United States > US
Switzerland
Massachusetts
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Abstract Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia (IH). Intercellular communication mediated by Connexins (Cx) regulates differentiation, growth and proliferation in various cell types. Microarray analysis of vein grafts in a model of bilateral rabbit jugular vein graft revealed Cx43 as an early upregulated gene. Additional experiments conducted using an ex-vivo human saphenous veins perfusion system (EVPS) confirmed that Cx43 was rapidly increased in human veins subjected ex-vivo to arterial hemodynamics. Cx43 knock-down by RNA interference, or adenoviral-mediated overexpression, respectively inhibited or stimulated the proliferation of primary human VSMC in vitro. Furthermore, Cx blockade with carbenoxolone or the specific Cx43 inhibitory peptide 43gap26 prevented the burst in myointimal proliferation and IH formation in human saphenous veins. Our data demonstrated that Cx43 controls proliferation and the formation of IH after arterial engraftment.
AbstractList Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia (IH). Intercellular communication mediated by Connexins (Cx) regulates differentiation, growth and proliferation in various cell types. Microarray analysis of vein grafts in a model of bilateral rabbit jugular vein graft revealed Cx43 as an early upregulated gene. Additional experiments conducted using an ex-vivo human saphenous veins perfusion system (EVPS) confirmed that Cx43 was rapidly increased in human veins subjected ex-vivo to arterial hemodynamics. Cx43 knock-down by RNA interference, or adenoviral-mediated overexpression, respectively inhibited or stimulated the proliferation of primary human VSMC in vitro. Furthermore, Cx blockade with carbenoxolone or the specific Cx43 inhibitory peptide .sup.43 gap26 prevented the burst in myointimal proliferation and IH formation in human saphenous veins. Our data demonstrated that Cx43 controls proliferation and the formation of IH after arterial engraftment.
Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia (IH). Intercellular communication mediated by Connexins (Cx) regulates differentiation, growth and proliferation in various cell types. Microarray analysis of vein grafts in a model of bilateral rabbit jugular vein graft revealed Cx43 as an early upregulated gene. Additional experiments conducted using an ex-vivo human saphenous veins perfusion system (EVPS) confirmed that Cx43 was rapidly increased in human veins subjected ex-vivo to arterial hemodynamics. Cx43 knock-down by RNA interference, or adenoviral-mediated overexpression, respectively inhibited or stimulated the proliferation of primary human VSMC in vitro . Furthermore, Cx blockade with carbenoxolone or the specific Cx43 inhibitory peptide 43 gap26 prevented the burst in myointimal proliferation and IH formation in human saphenous veins. Our data demonstrated that Cx43 controls proliferation and the formation of IH after arterial engraftment.
Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia (IH). Intercellular communication mediated by Connexins (Cx) regulates differentiation, growth and proliferation in various cell types. Microarray analysis of vein grafts in a model of bilateral rabbit jugular vein graft revealed Cx43 as an early upregulated gene. Additional experiments conducted using an ex-vivo human saphenous veins perfusion system (EVPS) confirmed that Cx43 was rapidly increased in human veins subjected ex-vivo to arterial hemodynamics. Cx43 knock-down by RNA interference, or adenoviral-mediated overexpression, respectively inhibited or stimulated the proliferation of primary human VSMC in vitro. Furthermore, Cx blockade with carbenoxolone or the specific Cx43 inhibitory peptide 43gap26 prevented the burst in myointimal proliferation and IH formation in human saphenous veins. Our data demonstrated that Cx43 controls proliferation and the formation of IH after arterial engraftment.
Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia (IH). Intercellular communication mediated by Connexins (Cx) regulates differentiation, growth and proliferation in various cell types. Microarray analysis of vein grafts in a model of bilateral rabbit jugular vein graft revealed Cx43 as an early upregulated gene. Additional experiments conducted using an ex-vivo human saphenous veins perfusion system (EVPS) confirmed that Cx43 was rapidly increased in human veins subjected ex-vivo to arterial hemodynamics. Cx43 knock-down by RNA interference, or adenoviral-mediated overexpression, respectively inhibited or stimulated the proliferation of primary human VSMC in vitro . Furthermore, Cx blockade with carbenoxolone or the specific Cx43 inhibitory peptide 43 gap26 prevented the burst in myointimal proliferation and IH formation in human saphenous veins. Our data demonstrated that Cx43 controls proliferation and the formation of IH after arterial engraftment.
Audience Academic
Author Berceli, Scott
Longchamp, Alban
Haefliger, Jacques-Antoine
Alonso, Florian
Dubuis, Céline
Mitchell, James R
Kuppler, Christopher
Allagnat, Florent
Ozaki, Charles-Keith
Corpataux, Jean-Marc
Déglise, Sébastien
AuthorAffiliation 1 Department of Vascular Surgery, Centre Hospitalier Universitaire Vaudois, Laboratory of Experimental Medicine, Lausanne, Switzerland
4 Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America
2 Department of Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
3 Malcom Randall Veterans Affairs Medical Center and the Division of Vascular and Endovascular Surgery, University of Florida College of Medicine, Gainesville, Florida, United States of America
National Institute of Health and Medical Research, FRANCE
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– name: National Institute of Health and Medical Research, FRANCE
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2015 Longchamp et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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– notice: 2015 Longchamp et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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DocumentTitleAlternate Connexin43 Controls Intimal Hyperplasia
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Competing Interests: The authors have declared that no competing interests exist.
Conceived and designed the experiments: AL F. Allagnat F. Alonso J-AH SD C-KO J-MC SB. Performed the experiments: AL F. Allagnat F. Alonso CK CD. Analyzed the data: AL F. Allagnat F. Alonso CK J-AH SD SB CD. Contributed reagents/materials/analysis tools: C-KO CK J-AH SD SB J-MC JM. Wrote the paper: AL F. Allagnat J-AH SD C-KO J-MC JM.
These authors contributed equally to this work as first authors.
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PublicationDate 2015-09-23
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PublicationDecade 2010
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SSID ssj0053866
Score 2.2947695
Snippet Venous bypass grafts often fail following arterial implantation due to excessive smooth muscle cells (VSMC) proliferation and consequent intimal hyperplasia...
SourceID plos
doaj
pubmedcentral
proquest
gale
crossref
pubmed
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
StartPage e0138847
SubjectTerms Analysis
Animals
Arteriosclerosis
Atherosclerosis
Biology
Carotid arteries
Cell Proliferation
Cell signaling
Connexin 43
Connexin 43 - antagonists & inhibitors
Connexin 43 - physiology
Connexins
DNA microarrays
Genetic aspects
Grafting
Grafts
Hemodynamics
Humans
Hyperplasia
Hyperplasia - prevention & control
Implantation
Jugular vein
Laboratories
Male
Medicine
Membrane proteins
Muscle, Smooth, Vascular - pathology
Muscles
Perfusion
Physiological aspects
Physiology
Prevention
Public health
Rabbits
Ribonucleic acid
Risk factors
RNA
RNA-mediated interference
Shear stress
Smooth muscle
Thrombosis
Tunica Intima - pathology
Vascular Grafting
Vascular surgery
Veins
Veins & arteries
Veins - transplantation
Womens health
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Title Connexin43 Inhibition Prevents Human Vein Grafts Intimal Hyperplasia
URI https://www.ncbi.nlm.nih.gov/pubmed/26398895
https://www.proquest.com/docview/1719303899
https://search.proquest.com/docview/1717484077
https://pubmed.ncbi.nlm.nih.gov/PMC4580578
https://doaj.org/article/5484fa6659054e86b9d6fc151b7a7d54
http://dx.doi.org/10.1371/journal.pone.0138847
Volume 10
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