Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells

Abstract The human airway epithelium lining the bronchial tree contains basal cells that proliferate, differentiate, and communicate with other components of their microenvironment. One method that cells use for intercellular communication involves the secretion of exosomes and other extracellular v...

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Autores principales:	Ashish Saxena, Matthew S. Walters, Jae-Hung Shieh, Ling-Bo Shen, Kazunori Gomi, Robert J. Downey, Ronald G. Crystal, Malcolm A. S. Moore
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/92449e126f694f7d8e77c16977597922
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spelling	oai:doaj.org-article:92449e126f694f7d8e77c169775979222021-12-02T11:39:27ZExtracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells10.1038/s41598-021-85534-62045-2322https://doaj.org/article/92449e126f694f7d8e77c169775979222021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85534-6https://doaj.org/toc/2045-2322Abstract The human airway epithelium lining the bronchial tree contains basal cells that proliferate, differentiate, and communicate with other components of their microenvironment. One method that cells use for intercellular communication involves the secretion of exosomes and other extracellular vesicles (EVs). We isolated exosome-enriched EVs that were produced from an immortalized human airway basal cell line (BCi-NS1.1) and found that their secretion is increased by exposure to cigarette smoke extract, suggesting that this stress stimulates release of EVs which could affect signaling to other cells. We have previously shown that primary human airway basal cells secrete vascular endothelial growth factor A (VEGFA) which can activate MAPK signaling cascades in endothelial cells via VEGF receptor–2 (VEGFR2). Here, we show that exposure of endothelial cells to exosome-enriched airway basal cell EVs promotes the survival of these cells and that this effect also involves VEGFR2 activation and is, at least in part, mediated by VEGFA present in the EVs. These observations demonstrate that EVs are involved in the intercellular signaling between airway basal cells and the endothelium which we previously reported. The downstream signaling pathways involved may be distinct and specific to the EVs, however, as increased phosphorylation of Akt, STAT3, p44/42 MAPK, and p38 MAPK was not seen following exposure of endothelial cells to airway basal cell EVs.Ashish SaxenaMatthew S. WaltersJae-Hung ShiehLing-Bo ShenKazunori GomiRobert J. DowneyRonald G. CrystalMalcolm A. S. MooreNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ashish Saxena Matthew S. Walters Jae-Hung Shieh Ling-Bo Shen Kazunori Gomi Robert J. Downey Ronald G. Crystal Malcolm A. S. Moore Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
description	Abstract The human airway epithelium lining the bronchial tree contains basal cells that proliferate, differentiate, and communicate with other components of their microenvironment. One method that cells use for intercellular communication involves the secretion of exosomes and other extracellular vesicles (EVs). We isolated exosome-enriched EVs that were produced from an immortalized human airway basal cell line (BCi-NS1.1) and found that their secretion is increased by exposure to cigarette smoke extract, suggesting that this stress stimulates release of EVs which could affect signaling to other cells. We have previously shown that primary human airway basal cells secrete vascular endothelial growth factor A (VEGFA) which can activate MAPK signaling cascades in endothelial cells via VEGF receptor–2 (VEGFR2). Here, we show that exposure of endothelial cells to exosome-enriched airway basal cell EVs promotes the survival of these cells and that this effect also involves VEGFR2 activation and is, at least in part, mediated by VEGFA present in the EVs. These observations demonstrate that EVs are involved in the intercellular signaling between airway basal cells and the endothelium which we previously reported. The downstream signaling pathways involved may be distinct and specific to the EVs, however, as increased phosphorylation of Akt, STAT3, p44/42 MAPK, and p38 MAPK was not seen following exposure of endothelial cells to airway basal cell EVs.
format	article
author	Ashish Saxena Matthew S. Walters Jae-Hung Shieh Ling-Bo Shen Kazunori Gomi Robert J. Downey Ronald G. Crystal Malcolm A. S. Moore
author_facet	Ashish Saxena Matthew S. Walters Jae-Hung Shieh Ling-Bo Shen Kazunori Gomi Robert J. Downey Ronald G. Crystal Malcolm A. S. Moore
author_sort	Ashish Saxena
title	Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
title_short	Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
title_full	Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
title_fullStr	Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
title_full_unstemmed	Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
title_sort	extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/92449e126f694f7d8e77c16977597922
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Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells

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