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Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima

A major factor contributing to failure of arteriovenous fistulas (AVFs) is migration of smooth muscle cells into the forming neointima. To identify the source of smooth muscle cells in neointima, we created end-to-end AVFs by anastomosing the common carotid artery to the jugular vein and studied neu...

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Autores principales: Liang, Ming, Wang, Yun, Liang, Anlin, Mitch, William E., Roy-Chaudhury, Prabir, Han, Guofeng, Cheng, Jizhong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4677993/
https://www.ncbi.nlm.nih.gov/pubmed/25786100
http://dx.doi.org/10.1038/ki.2015.73
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author Liang, Ming
Wang, Yun
Liang, Anlin
Mitch, William E.
Roy-Chaudhury, Prabir
Han, Guofeng
Cheng, Jizhong
author_facet Liang, Ming
Wang, Yun
Liang, Anlin
Mitch, William E.
Roy-Chaudhury, Prabir
Han, Guofeng
Cheng, Jizhong
author_sort Liang, Ming
collection PubMed
description A major factor contributing to failure of arteriovenous fistulas (AVFs) is migration of smooth muscle cells into the forming neointima. To identify the source of smooth muscle cells in neointima, we created end-to-end AVFs by anastomosing the common carotid artery to the jugular vein and studied neural crest-derived smooth muscle cells from the carotid artery which are Wnt1-positive during development. In Wnt1-cre-GFP mice, smooth muscle cells in the carotid artery but not the jugular vein are labeled with GFP. About half of the cells were GFP-positive in the neointima indicating their migration from the carotid artery to the jugular vein in AVFs created in these mice. Since fibroblast-specific protein-1 (FSP-1) regulates smooth muscle cell migration, we examined FSP-1 in failed AVFs and polytetrafluoroethylene (PTFE) grafts from patients with ESRD or from AVFs in mice with chronic kidney disease. In smooth muscle cells of AVFs or PTFE grafts, FSP-1 and activation of Notch1 are present. In smooth muscle cells, Notch1 increased RBP-Jκ transcription factor activity and RBP-Jκ stimulated FSP-1 expression. Conditional knockout of RBP-Jκ in smooth muscle cells or general knockout of FSP-1, suppressed neointima formation in AVFs in mice. Thus, the artery of AVFs is the major source of smooth muscle cells during neointima formation. Knockout of RBP-Jκ or FSP-1 ameliorates neointima formation and might improve AVF patency during long-term follow up.
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spelling pubmed-46779932016-03-01 Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima Liang, Ming Wang, Yun Liang, Anlin Mitch, William E. Roy-Chaudhury, Prabir Han, Guofeng Cheng, Jizhong Kidney Int Article A major factor contributing to failure of arteriovenous fistulas (AVFs) is migration of smooth muscle cells into the forming neointima. To identify the source of smooth muscle cells in neointima, we created end-to-end AVFs by anastomosing the common carotid artery to the jugular vein and studied neural crest-derived smooth muscle cells from the carotid artery which are Wnt1-positive during development. In Wnt1-cre-GFP mice, smooth muscle cells in the carotid artery but not the jugular vein are labeled with GFP. About half of the cells were GFP-positive in the neointima indicating their migration from the carotid artery to the jugular vein in AVFs created in these mice. Since fibroblast-specific protein-1 (FSP-1) regulates smooth muscle cell migration, we examined FSP-1 in failed AVFs and polytetrafluoroethylene (PTFE) grafts from patients with ESRD or from AVFs in mice with chronic kidney disease. In smooth muscle cells of AVFs or PTFE grafts, FSP-1 and activation of Notch1 are present. In smooth muscle cells, Notch1 increased RBP-Jκ transcription factor activity and RBP-Jκ stimulated FSP-1 expression. Conditional knockout of RBP-Jκ in smooth muscle cells or general knockout of FSP-1, suppressed neointima formation in AVFs in mice. Thus, the artery of AVFs is the major source of smooth muscle cells during neointima formation. Knockout of RBP-Jκ or FSP-1 ameliorates neointima formation and might improve AVF patency during long-term follow up. 2015-03-18 2015-09 /pmc/articles/PMC4677993/ /pubmed/25786100 http://dx.doi.org/10.1038/ki.2015.73 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Liang, Ming
Wang, Yun
Liang, Anlin
Mitch, William E.
Roy-Chaudhury, Prabir
Han, Guofeng
Cheng, Jizhong
Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima
title Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima
title_full Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima
title_fullStr Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima
title_full_unstemmed Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima
title_short Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima
title_sort migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires notch activation to form neointima
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4677993/
https://www.ncbi.nlm.nih.gov/pubmed/25786100
http://dx.doi.org/10.1038/ki.2015.73
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