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Impaired contractility and detrusor hypertrophy in cavin-1-deficient mice.

Karbalaei, Mardjaneh LU ; Rippe, Catarina LU ; Albinsson, Sebastian LU ; Ekman, Mari; Mansten, Alva; Uvelius, Bengt LU and Swärd, Karl LU (2012) In European Journal of Pharmacology 689(1-3). p.179-185
Abstract
Caveolae are membrane invaginations present in a variety of cell types. Formation of caveolae depends on caveolins and on the more recently discovered family of proteins known as the cavins. Genetic ablation of caveolin-1 was previously shown to give rise to a number of urogenital alterations, but the effects of cavin-1 deletion on urogenital function remain unknown. Here we characterized detrusor contractility and structure in cavin-1-deficient mice. Electron microscopy demonstrated essentially complete lack of caveolae in the knock-out detrusor, and immunoblotting disclosed reduced levels of cavin-3 and of all caveolin proteins. Bladder weight was increased in male knock-out mice, and length-tension relationships demonstrated a reduction... (More)
Caveolae are membrane invaginations present in a variety of cell types. Formation of caveolae depends on caveolins and on the more recently discovered family of proteins known as the cavins. Genetic ablation of caveolin-1 was previously shown to give rise to a number of urogenital alterations, but the effects of cavin-1 deletion on urogenital function remain unknown. Here we characterized detrusor contractility and structure in cavin-1-deficient mice. Electron microscopy demonstrated essentially complete lack of caveolae in the knock-out detrusor, and immunoblotting disclosed reduced levels of cavin-3 and of all caveolin proteins. Bladder weight was increased in male knock-out mice, and length-tension relationships demonstrated a reduction in depolarisation-induced contraction. Contractility in response to muscarinic receptor activation was similarly reduced. Despite these functional changes, micturition patterns were similar in conscious and freely moving animals and diuresis was unchanged. Our breeding additionally disclosed that the number of knock-out mice generated in heterozygous crosses was lower than expected, suggesting embryonic/perinatal lethality. In conclusion, this is the first study to show that cavin-1 is critical for detrusor caveolae and for the overall contractility and structure of the urinary bladder. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
European Journal of Pharmacology
volume
689
issue
1-3
pages
179 - 185
publisher
Elsevier
external identifiers
  • pmid:22643325
  • wos:000306646900025
  • scopus:84864285796
ISSN
1879-0712
DOI
10.1016/j.ejphar.2012.05.023
language
English
LU publication?
yes
id
be8c199a-847d-4404-8e2b-0d343395b142 (old id 2608317)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22643325?dopt=Abstract
date added to LUP
2012-06-04 21:14:43
date last changed
2017-08-27 03:36:39
@article{be8c199a-847d-4404-8e2b-0d343395b142,
  abstract     = {Caveolae are membrane invaginations present in a variety of cell types. Formation of caveolae depends on caveolins and on the more recently discovered family of proteins known as the cavins. Genetic ablation of caveolin-1 was previously shown to give rise to a number of urogenital alterations, but the effects of cavin-1 deletion on urogenital function remain unknown. Here we characterized detrusor contractility and structure in cavin-1-deficient mice. Electron microscopy demonstrated essentially complete lack of caveolae in the knock-out detrusor, and immunoblotting disclosed reduced levels of cavin-3 and of all caveolin proteins. Bladder weight was increased in male knock-out mice, and length-tension relationships demonstrated a reduction in depolarisation-induced contraction. Contractility in response to muscarinic receptor activation was similarly reduced. Despite these functional changes, micturition patterns were similar in conscious and freely moving animals and diuresis was unchanged. Our breeding additionally disclosed that the number of knock-out mice generated in heterozygous crosses was lower than expected, suggesting embryonic/perinatal lethality. In conclusion, this is the first study to show that cavin-1 is critical for detrusor caveolae and for the overall contractility and structure of the urinary bladder.},
  author       = {Karbalaei, Mardjaneh and Rippe, Catarina and Albinsson, Sebastian and Ekman, Mari and Mansten, Alva and Uvelius, Bengt and Swärd, Karl},
  issn         = {1879-0712},
  language     = {eng},
  number       = {1-3},
  pages        = {179--185},
  publisher    = {Elsevier},
  series       = {European Journal of Pharmacology},
  title        = {Impaired contractility and detrusor hypertrophy in cavin-1-deficient mice.},
  url          = {http://dx.doi.org/10.1016/j.ejphar.2012.05.023},
  volume       = {689},
  year         = {2012},
}