Sarcopenia is an age-related condition characterized by progressive loss of muscle strength and size. Research on muscle aging usually relies on aged mice, although they require great resources and expenses. This study evaluates Col6a1-/- mice as a potential alternative. Collagen VI plays crucial roles in skeletal muscle, and mutations of its genes are causative for congenital muscle diseases known as COL6-related myopathies. The research compares wild-type and knock-out mice at 6 and 18 months of age, focusing on two critical aspects of sarcopenia: the change in muscle size and the increased number of centralized nuclei within the fibers. These markers have been observed through staining of tibialis anterior muscle sections with Hematoxylin and Eosin, and wheat germ agglutinin (WGA) counterstained with Hoechst. Analysis of the fibers’ cross-sectional area and minimum Feret’s diameter revealed a significant change in small and large fibers’ diameter in 18 months Col6a1-/- mice compared to both younger and wild-type mice of the same age. Furthermore, results showed an increase of centralized nuclei in Col6a1-/- mice compared to the wild type, indicating muscle damage and ongoing regeneration. In conclusion, we have shown that Col6a1-/- mice resemble sarcopenic phenotype at an earlier age compared to wild-type mice.
Sarcopenia is an age-related condition characterized by progressive loss of muscle strength and size. Research on muscle aging usually relies on aged mice, although they require great resources and expenses. This study evaluates Col6a1-/- mice as a potential alternative. Collagen VI plays crucial roles in skeletal muscle, and mutations of its genes are causative for congenital muscle diseases known as COL6-related myopathies. The research compares wild-type and knock-out mice at 6 and 18 months of age, focusing on two critical aspects of sarcopenia: the change in muscle size and the increased number of centralized nuclei within the fibers. These markers have been observed through staining of tibialis anterior muscle sections with Hematoxylin and Eosin, and wheat germ agglutinin (WGA) counterstained with Hoechst. Analysis of the fibers’ cross-sectional area and minimum Feret’s diameter revealed a significant change in small and large fibers’ diameter in 18 months Col6a1-/- mice compared to both younger and wild-type mice of the same age. Furthermore, results showed an increase of centralized nuclei in Col6a1-/- mice compared to the wild type, indicating muscle damage and ongoing regeneration. In conclusion, we have shown that Col6a1-/- mice resemble sarcopenic phenotype at an earlier age compared to wild-type mice.
Evaluating Col6a1-/- mice as a model for sarcopenia: analysis of centralized nuclei and muscle fiber size
BATTINI, LUCIA
2023/2024
Abstract
Sarcopenia is an age-related condition characterized by progressive loss of muscle strength and size. Research on muscle aging usually relies on aged mice, although they require great resources and expenses. This study evaluates Col6a1-/- mice as a potential alternative. Collagen VI plays crucial roles in skeletal muscle, and mutations of its genes are causative for congenital muscle diseases known as COL6-related myopathies. The research compares wild-type and knock-out mice at 6 and 18 months of age, focusing on two critical aspects of sarcopenia: the change in muscle size and the increased number of centralized nuclei within the fibers. These markers have been observed through staining of tibialis anterior muscle sections with Hematoxylin and Eosin, and wheat germ agglutinin (WGA) counterstained with Hoechst. Analysis of the fibers’ cross-sectional area and minimum Feret’s diameter revealed a significant change in small and large fibers’ diameter in 18 months Col6a1-/- mice compared to both younger and wild-type mice of the same age. Furthermore, results showed an increase of centralized nuclei in Col6a1-/- mice compared to the wild type, indicating muscle damage and ongoing regeneration. In conclusion, we have shown that Col6a1-/- mice resemble sarcopenic phenotype at an earlier age compared to wild-type mice.File | Dimensione | Formato | |
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https://hdl.handle.net/20.500.12608/70506