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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Autores principales:	Jenq-Shyong Chan, Yang Wang, Virgilius Cornea, Prabir Roy-Chaudhury, Begoña Campos
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	adventitia macrophage proliferation arteriovenous fistula Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/dd63722cb7ef456588a2013f67974859
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spelling	oai:doaj.org-article:dd63722cb7ef456588a2013f679748592021-11-25T17:55:02ZEarly Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention10.3390/ijms2222122851422-00671661-6596https://doaj.org/article/dd63722cb7ef456588a2013f679748592021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12285https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Background: 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.Jenq-Shyong ChanYang WangVirgilius CorneaPrabir Roy-ChaudhuryBegoña CamposMDPI AGarticleadventitiamacrophageproliferationarteriovenous fistulaBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12285, p 12285 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	adventitia macrophage proliferation arteriovenous fistula Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	adventitia macrophage proliferation arteriovenous fistula Biology (General) QH301-705.5 Chemistry QD1-999 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
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.
format	article
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
title	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_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_sort	early adventitial activation and proliferation in a mouse model of arteriovenous stenosis: opportunities for intervention
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/dd63722cb7ef456588a2013f67974859
work_keys_str_mv	AT jenqshyongchan earlyadventitialactivationandproliferationinamousemodelofarteriovenousstenosisopportunitiesforintervention AT yangwang earlyadventitialactivationandproliferationinamousemodelofarteriovenousstenosisopportunitiesforintervention AT virgiliuscornea earlyadventitialactivationandproliferationinamousemodelofarteriovenousstenosisopportunitiesforintervention AT prabirroychaudhury earlyadventitialactivationandproliferationinamousemodelofarteriovenousstenosisopportunitiesforintervention AT begonacampos earlyadventitialactivationandproliferationinamousemodelofarteriovenousstenosisopportunitiesforintervention
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Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention

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