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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)
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author
organization
publishing date
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
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
2015-03-03 14:12:08
date last changed
2017-02-22 11:43:57
@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},
  volume       = {750},
  year         = {2015},
}