Vasopressin-induced mouse urethral contraction is modulated by caveolin-1.
Zeng, Jianwen LU ; Ekman, Mari LU ; Grossi, Mario LU ; Svensson, Daniel LU ; Nilsson, Bengt-Olof LU
; Jiang, Chonghe
; Uvelius, Bengt
LU
and Swärd, Karl
LU
(2015)
In European Journal of Pharmacology
750.
p.59-65
- Abstract
- Caveolae are 50-100nm large invaginations in the cell membrane that are considered to play roles in receptor signaling. Here we aimed to investigate the expression and distribution of the arginine-vasopressin (AVP) V1a receptor and its functional dependence on caveolin-1 (Cav1) in the mouse urethra. Female Cav1 knockout (KO) and wild type (WT) mice were used, and urethral preparations were micro-dissected for mechanical experiments. Methyl-β-cyclodextrin (mβcd) was used to deplete cholesterol and to disrupt caveolae. Protein expression and localization was determined using immunofluorescence and western blotting and transcript expression was determined by qRT-PCR. We found that Cav1 and AVP V1a receptors were expressed in urethral smooth... (More)
- Caveolae are 50-100nm large invaginations in the cell membrane that are considered to play roles in receptor signaling. Here we aimed to investigate the expression and distribution of the arginine-vasopressin (AVP) V1a receptor and its functional dependence on caveolin-1 (Cav1) in the mouse urethra. Female Cav1 knockout (KO) and wild type (WT) mice were used, and urethral preparations were micro-dissected for mechanical experiments. Methyl-β-cyclodextrin (mβcd) was used to deplete cholesterol and to disrupt caveolae. Protein expression and localization was determined using immunofluorescence and western blotting and transcript expression was determined by qRT-PCR. We found that Cav1 and AVP V1a receptors were expressed in urethral smooth muscle cells with apparent co-localization at the cell membrane. AVP caused urethral contraction that was inhibited by the V1a receptor antagonist SR49059. Concentration-response curves for AVP were right-shifted and maximal contraction was reduced in Cav1 KO mice and after mβcd treatment. In addition to caveolin-1 we also detected caveolin-2, cavin-1 and cavin-3 in the mouse urethra by western blotting. Caveolin-2, cavin-1 and cavin-3 as well as V1a receptor expression was reduced in KO urethra. We conclude that AVP regulates urethral contractility via the V1a receptor through a Cav1-dependent mechanism involving, in part, altered V1a receptor expression. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5145882
- author
- Zeng, Jianwen
LU
; Ekman, Mari
LU
; Grossi, Mario
LU
; Svensson, Daniel
LU
; Nilsson, Bengt-Olof
LU
; Jiang, Chonghe
; Uvelius, Bengt
LU
and Swärd, Karl
LU
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- European Journal of Pharmacology
- volume
- 750
- pages
- 59 - 65
- publisher
- Elsevier
- external identifiers
-
- pmid:25637087
- wos:000350389200010
- scopus:84922736058
- pmid:25637087
- ISSN
- 1879-0712
- DOI
- 10.1016/j.ejphar.2015.01.029
- language
- English
- LU publication?
- yes
- id
- 6d068f43-0598-4d1b-b581-c4b99447b245 (old id 5145882)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25637087?dopt=Abstract
- date added to LUP
- 2016-04-01 10:01:26
- date last changed
- 2022-01-25 19:00:38
@article{6d068f43-0598-4d1b-b581-c4b99447b245,
abstract = {{Caveolae are 50-100nm large invaginations in the cell membrane that are considered to play roles in receptor signaling. Here we aimed to investigate the expression and distribution of the arginine-vasopressin (AVP) V1a receptor and its functional dependence on caveolin-1 (Cav1) in the mouse urethra. Female Cav1 knockout (KO) and wild type (WT) mice were used, and urethral preparations were micro-dissected for mechanical experiments. Methyl-β-cyclodextrin (mβcd) was used to deplete cholesterol and to disrupt caveolae. Protein expression and localization was determined using immunofluorescence and western blotting and transcript expression was determined by qRT-PCR. We found that Cav1 and AVP V1a receptors were expressed in urethral smooth muscle cells with apparent co-localization at the cell membrane. AVP caused urethral contraction that was inhibited by the V1a receptor antagonist SR49059. Concentration-response curves for AVP were right-shifted and maximal contraction was reduced in Cav1 KO mice and after mβcd treatment. In addition to caveolin-1 we also detected caveolin-2, cavin-1 and cavin-3 in the mouse urethra by western blotting. Caveolin-2, cavin-1 and cavin-3 as well as V1a receptor expression was reduced in KO urethra. We conclude that AVP regulates urethral contractility via the V1a receptor through a Cav1-dependent mechanism involving, in part, altered V1a receptor expression.}},
author = {{Zeng, Jianwen and Ekman, Mari and Grossi, Mario and Svensson, Daniel and Nilsson, Bengt-Olof and Jiang, Chonghe and Uvelius, Bengt and Swärd, Karl}},
issn = {{1879-0712}},
language = {{eng}},
pages = {{59--65}},
publisher = {{Elsevier}},
series = {{European Journal of Pharmacology}},
title = {{Vasopressin-induced mouse urethral contraction is modulated by caveolin-1.}},
url = {{http://dx.doi.org/10.1016/j.ejphar.2015.01.029}},
doi = {{10.1016/j.ejphar.2015.01.029}},
volume = {{750}},
year = {{2015}},
}