Alterations of M-cadherin, neural cell adhesion molecule and beta-catenin expression in satellite cells during overload-induced skeletal muscle hypertrophy.

AIM: Neural cell adhesion molecule (NCAM) and M-cadherin are cell adhesion molecules expressed on the surface of skeletal muscle satellite cell (SC). During myogenic morphogenesis, M-cadherin participates in mediating terminal differentiation and fusion of myoblasts by forming a complex with beta-catenin and that NCAM contributes to myotube formation by fusion of myoblasts. Hypertrophy and hyperplasia of functionally overloaded skeletal muscle results from the fusion with SCs into the existing myofibres or new myofibre formation by SC-SC fusion. However, the alterations of NCAM, M-cadherin and beta-catenin expressions in SCs in response to functional overload have not been investigated.
METHODS: Using immunohistochemical approaches, we examined the temporal and spatial expression patterns of these factors expressed in SCs during the functional overload of skeletal muscles.
RESULTS: Myofibres with SCs showing NCAM+/M-cadherin-, NCAM+/M-cadherin+ or NCAM-/M-cadherin+ were detected in overloaded muscles. The percentage changes of myofibres with SCs showing NCAM+/M-cadherin-, NCAM+/M-cadherin+ or NCAM-/M-cadherin+ were elevated in day-3 post-overloaded muscles, and then only the percentage changes of myofibres with SCs showing NCAM-/M-cadherin+ were significantly increased in day-7 post-overload muscles (P < 0.05). Both beta-catenin and M-cadherin were co-localized throughout quiescent, proliferation and differentiation stages of SCs.
CONCLUSION: These results suggested that the expressions of NCAM, M-cadherin and beta-catenin in SCs may be controlled by distinct regulatory mechanisms during functional overload, and that interactions among NCAM, M-cadherin and beta-catenin in SCs may play important roles to contribute to overload-induced muscle hypertrophy via fusion with each other or into the existing myofibres of SCs.