Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.

Lung function declines as people age and their lungs become stiffer. With an increasing elderly population, understanding mechanisms that contribute to these structural and functional changes in the aging lung is important. Part of the aging process is characterized by thicker, more fibrotic airways...

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Autores principales:	Sarah A Wicher, Benjamin B Roos, Jacob J Teske, Yun Hua Fang, Christina Pabelick, Y S Prakash
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9ed70d7ed6a54bfd8c84a97a7475e3f6
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spelling	oai:doaj.org-article:9ed70d7ed6a54bfd8c84a97a7475e3f62021-12-02T20:08:57ZAging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.1932-620310.1371/journal.pone.0254710https://doaj.org/article/9ed70d7ed6a54bfd8c84a97a7475e3f62021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0254710https://doaj.org/toc/1932-6203Lung function declines as people age and their lungs become stiffer. With an increasing elderly population, understanding mechanisms that contribute to these structural and functional changes in the aging lung is important. Part of the aging process is characterized by thicker, more fibrotic airways, and senile emphysema caused by changes in lung parenchyma. There is also senescence, which occurs throughout the body with aging. Here, using human airway smooth muscle (ASM) cells from patients in different age groups, we explored senescence pathways and changes in intracellular calcium signaling and extracellular matrix (ECM) deposition to elucidate potential mechanisms by which aging leads to thicker and stiffer lungs. Senescent markers p21, γH2AX, and β-gal, and some senescence-associated secretory proteins (SASP) increased with aging, as shown by staining and biochemical analyses. Agonist-induced intracellular Ca2+ responses, measured using fura-2 loaded cells and fluorescence imaging, increased with age. However, biochemical analysis showed that expression of the following markers decreased with age: M3 muscarinic receptor, TRPC3, Orai1, STIM1, SERCA2, MMP2 and MMP9. In contrast, collagen III, and fibronectin deposition increased with age. These data show that senescence increases in the aging airways that is associated with a stiffer but surprisingly greater intracellular calcium signaling as a marker for contractility. ASM senescence may enhance fibrosis in a feed forward loop promoting remodeling and altered calcium storage and buffering.Sarah A WicherBenjamin B RoosJacob J TeskeYun Hua FangChristina PabelickY S PrakashPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 7, p e0254710 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sarah A Wicher Benjamin B Roos Jacob J Teske Yun Hua Fang Christina Pabelick Y S Prakash Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
description	Lung function declines as people age and their lungs become stiffer. With an increasing elderly population, understanding mechanisms that contribute to these structural and functional changes in the aging lung is important. Part of the aging process is characterized by thicker, more fibrotic airways, and senile emphysema caused by changes in lung parenchyma. There is also senescence, which occurs throughout the body with aging. Here, using human airway smooth muscle (ASM) cells from patients in different age groups, we explored senescence pathways and changes in intracellular calcium signaling and extracellular matrix (ECM) deposition to elucidate potential mechanisms by which aging leads to thicker and stiffer lungs. Senescent markers p21, γH2AX, and β-gal, and some senescence-associated secretory proteins (SASP) increased with aging, as shown by staining and biochemical analyses. Agonist-induced intracellular Ca2+ responses, measured using fura-2 loaded cells and fluorescence imaging, increased with age. However, biochemical analysis showed that expression of the following markers decreased with age: M3 muscarinic receptor, TRPC3, Orai1, STIM1, SERCA2, MMP2 and MMP9. In contrast, collagen III, and fibronectin deposition increased with age. These data show that senescence increases in the aging airways that is associated with a stiffer but surprisingly greater intracellular calcium signaling as a marker for contractility. ASM senescence may enhance fibrosis in a feed forward loop promoting remodeling and altered calcium storage and buffering.
format	article
author	Sarah A Wicher Benjamin B Roos Jacob J Teske Yun Hua Fang Christina Pabelick Y S Prakash
author_facet	Sarah A Wicher Benjamin B Roos Jacob J Teske Yun Hua Fang Christina Pabelick Y S Prakash
author_sort	Sarah A Wicher
title	Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
title_short	Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
title_full	Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
title_fullStr	Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
title_full_unstemmed	Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
title_sort	aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/9ed70d7ed6a54bfd8c84a97a7475e3f6
work_keys_str_mv	AT sarahawicher agingincreasessenescencecalciumsignalingandextracellularmatrixdepositioninhumanairwaysmoothmuscle AT benjaminbroos agingincreasessenescencecalciumsignalingandextracellularmatrixdepositioninhumanairwaysmoothmuscle AT jacobjteske agingincreasessenescencecalciumsignalingandextracellularmatrixdepositioninhumanairwaysmoothmuscle AT yunhuafang agingincreasessenescencecalciumsignalingandextracellularmatrixdepositioninhumanairwaysmoothmuscle AT christinapabelick agingincreasessenescencecalciumsignalingandextracellularmatrixdepositioninhumanairwaysmoothmuscle AT ysprakash agingincreasessenescencecalciumsignalingandextracellularmatrixdepositioninhumanairwaysmoothmuscle
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Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle.

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