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Altered mechanical properties in smooth muscle of mice with a mutated calponin locus
Ayako Fujishige1, Katsuhito Takahashi, Teizo Tsuchiya
1Department of Biology, Faculty of Science, Kobe University, Rokkodai, Nada-ku, Kobe 657-8501, Japan.
Abstract:
The mechanical properties of smooth muscles in aorta and vas deferens were studied in mice with a mutated basic calponin locus to learn the physiological function of calponin. The intact smooth muscles were stimulated with high KCl and the force development was compared between calponin deficient (knockout, KO) mice and wild type (WT) ones. The isometric force induced by various concentrations of high KCl was lower in KO than in WT both in aorta and in vas deferens. The length-force relations were compared between KO and WT. The active isometric force in KO was significantly lower at most muscle lengths examined than in WT without the change in resting force both in aorta and in vas deferens. In vas deferens, the rate of force development after quick release in length at the peak force was significantly faster in KO than in WT. The above results show that the force development is lower and the rate of cross-bridge cycle is faster in KO mice than in WT ones, suggesting that calponin plays basic roles in the control of the contraction of smooth muscle.
Insights
Calponin deficiency in mice reduces smooth muscle force but speeds up cross-bridge cycling. This suggests calponin is crucial for regulating smooth muscle contraction in aorta and vas deferens.
Area of Science:
- Physiology
- Biochemistry
- Molecular Biology
Background:
- Calponin is a protein found in smooth muscle.
- Its exact physiological function remains largely unknown.
- Understanding calponin's role is key to smooth muscle physiology.
Purpose of the Study:
- To investigate the physiological function of calponin.
- To determine calponin's role in smooth muscle contraction.
- To compare mechanical properties of smooth muscles in calponin-deficient mice.
Main Methods:
- Studied mechanical properties of aorta and vas deferens smooth muscles in calponin knockout (KO) mice and wild-type (WT) mice.
- Stimulated intact smooth muscles with high potassium chloride (KCl).
- Compared isometric force development and length-force relations between KO and WT mice.
Main Results:
- Isometric force development was significantly lower in KO mice compared to WT mice in both aorta and vas deferens.
- Active isometric force was reduced in KO mice across most muscle lengths without affecting resting force.
- The rate of force development after quick release was faster in the vas deferens of KO mice.
Conclusions:
- Calponin deficiency leads to reduced force generation in smooth muscle.
- Calponin-deficient smooth muscle exhibits a faster cross-bridge cycle rate.
- These findings indicate calponin plays a fundamental role in controlling smooth muscle contraction.
