Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal

Bladder disorders associated with interstitial cystitis are frequently characterized by increased contractility and pain. The goals of this study were to examine 1) the effects of blocking proteinase-activated receptor-2 (PAR2) on the exaggerated bladder activity and pain evoked by cystitis and 2) t...

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Autores principales:	Chen Daihui, Liu Nian, Li Mao, Liang Simin
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2016
Materias:	bladder activity cystic pain cystitis proteinase-activated receptor-2 (par2) transient receptor potential a1 (trpa1) Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/9cc8894ead3f4c6486f832611a155ec4
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spelling	oai:doaj.org-article:9cc8894ead3f4c6486f832611a155ec42021-12-05T14:11:04ZBlocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal2081-693610.1515/tnsci-2016-0020https://doaj.org/article/9cc8894ead3f4c6486f832611a155ec42016-01-01T00:00:00Zhttps://doi.org/10.1515/tnsci-2016-0020https://doaj.org/toc/2081-6936Bladder disorders associated with interstitial cystitis are frequently characterized by increased contractility and pain. The goals of this study were to examine 1) the effects of blocking proteinase-activated receptor-2 (PAR2) on the exaggerated bladder activity and pain evoked by cystitis and 2) the underlying mechanisms responsible for the role of PAR2 in regulating cystic sensory activity. The protein expression of PAR2 was amplified in rats with cystitis by inducing it with systemic administration of cyclophosphamide (CYP) as compared with control rats. Blocking PAR2 by intrathecal infusion of PAR2 antagonist FSLLRY-NH2 attenuated bladder hyperactivity and pain. In addition, blocking PAR2 attenuated the transient receptor potential A1 (TRPA1) signal pathway, whereas inhibition of the TRPA1 decreased bladder hyperactivity and pain. The data revealed specific signaling pathways leading to CYP-induced bladder hyperactivity and pain, including the activation of PAR2 and TRPA1. Inhibition of these pathways alleviates cystic pain. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of overactive bladder and pain often observed in cystitis.Chen DaihuiLiu NianLi MaoLiang SiminDe Gruyterarticlebladder activitycystic paincystitisproteinase-activated receptor-2 (par2)transient receptor potential a1 (trpa1)Neurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENTranslational Neuroscience, Vol 7, Iss 1, Pp 133-138 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	bladder activity cystic pain cystitis proteinase-activated receptor-2 (par2) transient receptor potential a1 (trpa1) Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	bladder activity cystic pain cystitis proteinase-activated receptor-2 (par2) transient receptor potential a1 (trpa1) Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Chen Daihui Liu Nian Li Mao Liang Simin Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal
description	Bladder disorders associated with interstitial cystitis are frequently characterized by increased contractility and pain. The goals of this study were to examine 1) the effects of blocking proteinase-activated receptor-2 (PAR2) on the exaggerated bladder activity and pain evoked by cystitis and 2) the underlying mechanisms responsible for the role of PAR2 in regulating cystic sensory activity. The protein expression of PAR2 was amplified in rats with cystitis by inducing it with systemic administration of cyclophosphamide (CYP) as compared with control rats. Blocking PAR2 by intrathecal infusion of PAR2 antagonist FSLLRY-NH2 attenuated bladder hyperactivity and pain. In addition, blocking PAR2 attenuated the transient receptor potential A1 (TRPA1) signal pathway, whereas inhibition of the TRPA1 decreased bladder hyperactivity and pain. The data revealed specific signaling pathways leading to CYP-induced bladder hyperactivity and pain, including the activation of PAR2 and TRPA1. Inhibition of these pathways alleviates cystic pain. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of overactive bladder and pain often observed in cystitis.
format	article
author	Chen Daihui Liu Nian Li Mao Liang Simin
author_facet	Chen Daihui Liu Nian Li Mao Liang Simin
author_sort	Chen Daihui
title	Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal
title_short	Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal
title_full	Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal
title_fullStr	Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal
title_full_unstemmed	Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal
title_sort	blocking par2 alleviates bladder pain and hyperactivity via trpa1 signal
publisher	De Gruyter
publishDate	2016
url	https://doaj.org/article/9cc8894ead3f4c6486f832611a155ec4
work_keys_str_mv	AT chendaihui blockingpar2alleviatesbladderpainandhyperactivityviatrpa1signal AT liunian blockingpar2alleviatesbladderpainandhyperactivityviatrpa1signal AT limao blockingpar2alleviatesbladderpainandhyperactivityviatrpa1signal AT liangsimin blockingpar2alleviatesbladderpainandhyperactivityviatrpa1signal
_version_	1718371436948619264

Blocking PAR2 alleviates bladder pain and hyperactivity via TRPA1 signal

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