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Caveolin-3 differentially orchestrates cholinergic and serotonergic constriction of murine airways.

Abstract：

:The mechanisms of controlling airway smooth muscle (ASM) tone are of utmost clinical importance as inappropriate constriction is a hallmark in asthma and chronic obstructive pulmonary disease. Receptors for acetylcholine and serotonin, two relevant mediators in this context, appear to be incorporated in specialized, cholesterol-rich domains of the plasma membrane, termed caveolae due to their invaginated shape. The structural protein caveolin-1 partly accounts for anchoring of these receptors. We here determined the role of the other major caveolar protein, caveolin-3 (cav-3), in orchestrating cholinergic and serotonergic ASM responses, utilizing newly generated cav-3 deficient mice. Cav-3 deficiency fully abrogated serotonin-induced constriction of extrapulmonary airways in organ baths while leaving intrapulmonary airways unaffected, as assessed in precision cut lung slices. The selective expression of cav-3 in tracheal, but not intrapulmonary bronchial epithelial cells, revealed by immunohistochemistry, might explain the differential effects of cav-3 deficiency on serotonergic ASM constriction. The cholinergic response of extrapulmonary airways was not altered, whereas a considerable increase was observed in cav-3-/- intrapulmonary bronchi. Thus, cav-3 differentially organizes serotonergic and cholinergic signaling in ASM through mechanisms that are specific for airways of certain caliber and anatomical position. This may allow for selective and site-specific intervention in hyperreactive states.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Keshavarz M,Skill M,Hollenhorst MI,Maxeiner S,Walecki M,Pfeil U,Kummer W,Krasteva-Christ G

doi

10.1038/s41598-018-25445-1

subject

Has Abstract

pub_date

2018-05-14 00:00:00

pages

7508

issue

1

issn

2045-2322

pii

10.1038/s41598-018-25445-1

journal_volume

8

pub_type

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