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Impaired contractility and detrusor hypertrophy in cavin-1-deficient mice
Mardjaneh Sadegh Karbalaei1, Catarina Rippe, Sebastian Albinsson
1Department of Experimental Medical Science, Lund University, Biomedical Centre, BMC D12, SE-221 84 Lund, Sweden.
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 characterised 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.
Insights
Cavin-1 deficiency eliminates bladder caveolae, impairing detrusor muscle contractility and structure. This study reveals cavin-1
Area of Science:
- Cell biology
- Urology
- Physiology
Background:
- Caveolae are essential membrane structures involved in cellular processes.
- Caveolin proteins and the cavin family are critical for caveolae formation.
- The role of cavin-1 in urogenital function was previously uncharacterized.
Purpose of the Study:
- To investigate the role of cavin-1 in urinary bladder structure and function.
- To characterize detrusor contractility and morphology in cavin-1-deficient mice.
Main Methods:
- Generation and analysis of cavin-1-deficient mice.
- Electron microscopy to assess caveolae formation.
- Immunoblotting to evaluate protein levels.
- Functional assays to measure detrusor contractility.
Main Results:
- Cavin-1 deficiency resulted in a near-complete absence of caveolae in the detrusor.
- Reduced expression of cavin-3 and caveolin proteins was observed.
- Bladder weight increased in male knockout mice.
- Detrusor contractility was impaired in response to depolarization and muscarinic receptor activation.
- Micturition patterns and diuresis remained unchanged in conscious animals.
- Reduced numbers of knockout mice suggested embryonic/perinatal lethality.
Conclusions:
- Cavin-1 is essential for the formation of caveolae in the urinary bladder detrusor.
- Cavin-1 plays a critical role in regulating detrusor muscle contractility and structure.
- Cavin-1 deficiency may lead to embryonic/perinatal lethality.
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