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Apoptosis and apoptosis-related proteins in thyroid myopathies
Maria C Monici1, Carmelo Rodolico, Antonio Toscano
1Clinica Neurologia 2, Department of Neurosciences, Psychiatry and Anaesthesiology, Policlinico Universitario, 98125 Messina, Italy.
Abstract:
DNA fragmentation and apoptosis-related proteins have been investigated in thyroid cells and there is evidence that Fas-mediated apoptosis is inhibited by thyroid stimulating hormone (TSH). We investigated DNA fragmentation by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and Bcl-2 and Fas antigen expression by immunocytochemistry in skeletal muscles from 12 patients with hypothyroid myopathy and 5 patients with hyperthyroid myopathy. The finding of very few TUNEL-positive muscle fibers in both conditions suggests that apoptosis does not play a role in the pathogenesis of thyroid myopathies. Bcl-2 expression increased significantly in hypothyroid myopathy, correlating with high serum TSH levels, and not with either triiodothyronine (T3) or thyroxine (T4) serum levels. By contrast, Fas antigen was overexpressed in hyperthyroid myopathy, correlating with low TSH levels. These findings suggest an anti-apoptotic role for TSH itself in skeletal muscle.
Insights
Thyroid stimulating hormone (TSH) may protect skeletal muscles from cell death. This study found TSH influences apoptosis-related proteins in thyroid myopathies, suggesting an anti-apoptotic role for TSH in muscle.
Area of Science:
- Endocrinology
- Cell Biology
- Muscle Physiology
Background:
- Thyroid hormones significantly impact skeletal muscle function.
- Thyroid stimulating hormone (TSH) is known to influence thyroid cell apoptosis.
- The role of TSH in skeletal muscle apoptosis is not well understood.
Purpose of the Study:
- To investigate the role of apoptosis in the pathogenesis of hypothyroid and hyperthyroid myopathies.
- To examine the expression of apoptosis-related proteins, Bcl-2 and Fas antigen, in skeletal muscle of patients with thyroid myopathies.
- To determine the correlation between these protein expressions and serum levels of TSH, triiodothyronine (T3), and thyroxine (T4).
Main Methods:
- Skeletal muscle samples were obtained from 12 patients with hypothyroid myopathy and 5 with hyperthyroid myopathy.
- DNA fragmentation was assessed using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.
- Bcl-2 and Fas antigen expression levels were determined by immunocytochemistry.
Main Results:
- Apoptosis, indicated by TUNEL-positive muscle fibers, was minimal in both hypothyroid and hyperthyroid myopathies.
- Bcl-2 expression was significantly elevated in hypothyroid myopathy, correlating positively with high serum TSH levels.
- Fas antigen was overexpressed in hyperthyroid myopathy, correlating with low TSH levels.
Conclusions:
- Apoptosis does not appear to be a major factor in the development of thyroid myopathies.
- TSH may exert an anti-apoptotic effect on skeletal muscle tissue.
- The findings suggest a direct role for TSH in regulating muscle cell survival, independent of T3 and T4 levels.