Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.

Uncontrolled proliferation of endothelial cells is essential to the pathogenesis of pulmonary arterial hypertension (PAH). Both proliferation and cytoskeleton reorganization are associated with upregulation of the intermediate filament protein Nestin. Recently, accumulation of Nestin-expressing cell...

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Autores principales:	Aneel R Bhagwani, Schuyler Hultman, Daniela Farkas, Rebecca Moncayo, Kaivalya Dandamudi, Arsema K Zadu, Carlyne D Cool, Laszlo Farkas
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2019
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e8c8ed75ac6245148dd33db36adf9bfa
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spelling	oai:doaj.org-article:e8c8ed75ac6245148dd33db36adf9bfa2021-12-02T20:11:30ZEndothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.1932-620310.1371/journal.pone.0213890https://doaj.org/article/e8c8ed75ac6245148dd33db36adf9bfa2019-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0213890https://doaj.org/toc/1932-6203Uncontrolled proliferation of endothelial cells is essential to the pathogenesis of pulmonary arterial hypertension (PAH). Both proliferation and cytoskeleton reorganization are associated with upregulation of the intermediate filament protein Nestin. Recently, accumulation of Nestin-expressing cells was found in pulmonary vascular lesions of PAH patients. The goal of this study is to determine if Nestin expression contributes to endothelial proliferation in pulmonary arterial hypertension, using both lung tissues and endothelial cells. Here we found that endothelial cells from complex and plexiform lesions of PAH patients expressed Nestin. These Nestin+ cells further stained positive for the angiogenic factors CXC chemokine ligand 12 and Wnt1. Likewise, in the chronic hypoxia/SU5416 animal model of pulmonary hypertension, Nestin+ endothelial cells were found in occlusive pulmonary vascular lesions. In vitro, both growing rat and human lung endothelial cells expressed Nestin protein. When Nestin was overexpressed in endothelial cells (both rat and human), Nestin overexpression promoted proliferation and expression of CXC chemokine ligand 12. Nestin overexpression further increased angiogenic tube formation in vitro. Conclusions: We found increased Nestin expression from endothelial cells of occlusive lung vascular lesions in severe pulmonary hypertension. Elevated Nestin expression likely contributes to unchecked pulmonary vascular proliferation and angiogenesis, possibly via induction of CXC chemokine ligand 12. Additional studies are required to determine whether targeting Nestin would be beneficial to treat PAH.Aneel R BhagwaniSchuyler HultmanDaniela FarkasRebecca MoncayoKaivalya DandamudiArsema K ZaduCarlyne D CoolLaszlo FarkasPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 14, Iss 3, p e0213890 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Aneel R Bhagwani Schuyler Hultman Daniela Farkas Rebecca Moncayo Kaivalya Dandamudi Arsema K Zadu Carlyne D Cool Laszlo Farkas Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.
description	Uncontrolled proliferation of endothelial cells is essential to the pathogenesis of pulmonary arterial hypertension (PAH). Both proliferation and cytoskeleton reorganization are associated with upregulation of the intermediate filament protein Nestin. Recently, accumulation of Nestin-expressing cells was found in pulmonary vascular lesions of PAH patients. The goal of this study is to determine if Nestin expression contributes to endothelial proliferation in pulmonary arterial hypertension, using both lung tissues and endothelial cells. Here we found that endothelial cells from complex and plexiform lesions of PAH patients expressed Nestin. These Nestin+ cells further stained positive for the angiogenic factors CXC chemokine ligand 12 and Wnt1. Likewise, in the chronic hypoxia/SU5416 animal model of pulmonary hypertension, Nestin+ endothelial cells were found in occlusive pulmonary vascular lesions. In vitro, both growing rat and human lung endothelial cells expressed Nestin protein. When Nestin was overexpressed in endothelial cells (both rat and human), Nestin overexpression promoted proliferation and expression of CXC chemokine ligand 12. Nestin overexpression further increased angiogenic tube formation in vitro. Conclusions: We found increased Nestin expression from endothelial cells of occlusive lung vascular lesions in severe pulmonary hypertension. Elevated Nestin expression likely contributes to unchecked pulmonary vascular proliferation and angiogenesis, possibly via induction of CXC chemokine ligand 12. Additional studies are required to determine whether targeting Nestin would be beneficial to treat PAH.
format	article
author	Aneel R Bhagwani Schuyler Hultman Daniela Farkas Rebecca Moncayo Kaivalya Dandamudi Arsema K Zadu Carlyne D Cool Laszlo Farkas
author_facet	Aneel R Bhagwani Schuyler Hultman Daniela Farkas Rebecca Moncayo Kaivalya Dandamudi Arsema K Zadu Carlyne D Cool Laszlo Farkas
author_sort	Aneel R Bhagwani
title	Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.
title_short	Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.
title_full	Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.
title_fullStr	Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.
title_full_unstemmed	Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.
title_sort	endothelial cells are a source of nestin expression in pulmonary arterial hypertension.
publisher	Public Library of Science (PLoS)
publishDate	2019
url	https://doaj.org/article/e8c8ed75ac6245148dd33db36adf9bfa
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Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.

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