Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention

Background: Arteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AV...

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Main Authors: Jenq-Shyong Chan, Yang Wang, Virgilius Cornea, Prabir Roy-Chaudhury, Begoña Campos
Format: Article
Language:English
Published: MDPI AG 2021-11-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/22/22/12285
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author Jenq-Shyong Chan
Yang Wang
Virgilius Cornea
Prabir Roy-Chaudhury
Begoña Campos
author_facet Jenq-Shyong Chan
Yang Wang
Virgilius Cornea
Prabir Roy-Chaudhury
Begoña Campos
author_sort Jenq-Shyong Chan
collection DOAJ
description Background: Arteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AVF stenosis. Methods: Standard immunohistochemical analyses for cellular proliferation and macrophage infiltration were performed at 2, 7 and 14 d on our validated mouse model of AVF stenosis to study the temporal profile, geographical location and cellular phenotype of proliferating and infiltrating cells in this model. Results: Adventitial proliferation and macrophage infiltration (into the adventitia) began at 2 d, peaked at 7 d and then declined over time. Surprisingly, there was minimal macrophage infiltration or proliferation in the neointimal region at either 7 or 14 d, although endothelial cell proliferation increased rapidly between 2 d and 7 d, and peaked at 14 d. Conclusions: Early and rapid macrophage infiltration and cellular proliferation within the adventitia could play an important role in the downstream pathways of both neointimal hyperplasia and inward or outward remodelling.
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spelling doaj.art-dd63722cb7ef456588a2013f679748592023-11-22T23:39:56ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-11-0122221228510.3390/ijms222212285Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for InterventionJenq-Shyong Chan0Yang Wang1Virgilius Cornea2Prabir Roy-Chaudhury3Begoña Campos4Division of Nephrology, Department of Internal Medicine, Armed Forces Taoyuan General Hospital, Taoyuan 325, TaiwanDivision of Nephrology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH 45267, USADepartment of Pathology, University of Cincinnati, Cincinnati, OH 45267, USADepartment of Medicine, Division of Nephrology and Hypertension, University of North Carolina, Chapel Hill, NC 27599, USADivision of Nephrology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH 45267, USABackground: Arteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AVF stenosis. Methods: Standard immunohistochemical analyses for cellular proliferation and macrophage infiltration were performed at 2, 7 and 14 d on our validated mouse model of AVF stenosis to study the temporal profile, geographical location and cellular phenotype of proliferating and infiltrating cells in this model. Results: Adventitial proliferation and macrophage infiltration (into the adventitia) began at 2 d, peaked at 7 d and then declined over time. Surprisingly, there was minimal macrophage infiltration or proliferation in the neointimal region at either 7 or 14 d, although endothelial cell proliferation increased rapidly between 2 d and 7 d, and peaked at 14 d. Conclusions: Early and rapid macrophage infiltration and cellular proliferation within the adventitia could play an important role in the downstream pathways of both neointimal hyperplasia and inward or outward remodelling.https://www.mdpi.com/1422-0067/22/22/12285adventitiamacrophageproliferationarteriovenous fistula
spellingShingle Jenq-Shyong Chan
Yang Wang
Virgilius Cornea
Prabir Roy-Chaudhury
Begoña Campos
Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention
International Journal of Molecular Sciences
adventitia
macrophage
proliferation
arteriovenous fistula
title Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention
title_full Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention
title_fullStr Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention
title_full_unstemmed Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention
title_short Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention
title_sort early adventitial activation and proliferation in a mouse model of arteriovenous stenosis opportunities for intervention
topic adventitia
macrophage
proliferation
arteriovenous fistula
url https://www.mdpi.com/1422-0067/22/22/12285
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AT virgiliuscornea earlyadventitialactivationandproliferationinamousemodelofarteriovenousstenosisopportunitiesforintervention
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