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Thyroid hormones up-regulate Ca-channels in cultured skeletal muscle of the rat
1Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
Abstract:
The effects of thyroid hormones (TH) were examined on the expression of slow Ca2(+)-channels in cultures of rat skeletal muscle. Myotubes were treated with TH at age 5-7 days in vitro, and measurements of specific binding of the dihydropyridine Ca-channel antagonist [3H]PN200-110 were made beginning 12 h later. TH caused a dose-related increase in PN200-110 binding sites with a lower affinity for the ligand than in control cells. The effect was blocked by simultaneous treatment with cycloheximide or actinomycin-D. The results indicate that TH increase gene expression of slow Ca2(+)-channels of skeletal muscle.
Insights
Thyroid hormones (TH) increase the gene expression of slow calcium channels in rat skeletal muscle cells. This finding suggests TH play a crucial role in regulating muscle cell function.
Area of Science:
- Molecular Biology
- Endocrinology
- Muscle Physiology
Background:
- Thyroid hormones (TH) are critical regulators of metabolism and development.
- Calcium channels play vital roles in muscle contraction and cellular signaling.
- The specific effects of TH on skeletal muscle calcium channel expression remain incompletely understood.
Purpose of the Study:
- To investigate the impact of thyroid hormones on the expression of slow calcium channels in cultured rat skeletal muscle cells.
- To determine if TH modulate the number or function of dihydropyridine-sensitive calcium channels.
Main Methods:
- Primary cultures of rat skeletal muscle myotubes were established.
- Myotubes were treated with varying concentrations of thyroid hormones.
- The binding of a specific dihydropyridine calcium channel antagonist ([3H]PN200-110) was measured to quantify channel expression.
- The role of protein synthesis and gene transcription was assessed using cycloheximide and actinomycin-D.
Main Results:
- Thyroid hormone treatment resulted in a dose-dependent increase in the number of [3H]PN200-110 binding sites.
- The affinity of the calcium channels for the antagonist was reduced in TH-treated cells.
- The observed increase in binding sites was abrogated by cycloheximide and actinomycin-D, indicating a requirement for new protein synthesis and gene expression.
- These findings suggest TH upregulate the gene expression of slow calcium channels.
Conclusions:
- Thyroid hormones enhance the gene expression of slow calcium channels in skeletal muscle.
- TH signaling is important for regulating the abundance of functional calcium channels in muscle cells.
- This mechanism may contribute to the overall effects of thyroid hormones on skeletal muscle physiology.