Cargando…

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

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 (...

Descripción completa

Detalles Bibliográficos
Autores principales: Saxena, Ashish, Walters, Matthew S., Shieh, Jae-Hung, Shen, Ling-Bo, Gomi, Kazunori, Downey, Robert J., Crystal, Ronald G., Moore, Malcolm A. S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7969738/
https://www.ncbi.nlm.nih.gov/pubmed/33731767
http://dx.doi.org/10.1038/s41598-021-85534-6
_version_ 1783666286830551040
author Saxena, Ashish
Walters, Matthew S.
Shieh, Jae-Hung
Shen, Ling-Bo
Gomi, Kazunori
Downey, Robert J.
Crystal, Ronald G.
Moore, Malcolm A. S.
author_facet Saxena, Ashish
Walters, Matthew S.
Shieh, Jae-Hung
Shen, Ling-Bo
Gomi, Kazunori
Downey, Robert J.
Crystal, Ronald G.
Moore, Malcolm A. S.
author_sort Saxena, Ashish
collection PubMed
description 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 Online
Article
Text
id pubmed-7969738
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Nature Publishing Group UK
record_format MEDLINE/PubMed
spelling pubmed-79697382021-03-19 Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells Saxena, Ashish Walters, Matthew S. Shieh, Jae-Hung Shen, Ling-Bo Gomi, Kazunori Downey, Robert J. Crystal, Ronald G. Moore, Malcolm A. S. Sci Rep Article 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. Nature Publishing Group UK 2021-03-17 /pmc/articles/PMC7969738/ /pubmed/33731767 http://dx.doi.org/10.1038/s41598-021-85534-6 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Saxena, Ashish
Walters, Matthew S.
Shieh, Jae-Hung
Shen, Ling-Bo
Gomi, Kazunori
Downey, Robert J.
Crystal, Ronald G.
Moore, Malcolm A. S.
Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells
title 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_short 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
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7969738/
https://www.ncbi.nlm.nih.gov/pubmed/33731767
http://dx.doi.org/10.1038/s41598-021-85534-6
work_keys_str_mv AT saxenaashish extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT waltersmatthews extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT shiehjaehung extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT shenlingbo extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT gomikazunori extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT downeyrobertj extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT crystalronaldg extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells
AT mooremalcolmas extracellularvesiclesfromhumanairwaybasalcellsrespondtocigarettesmokeextractandaffectvascularendothelialcells