Question: 

Transient receptor potential (TRP) channels are expressed in mammalian skeletal muscle and are known to influence muscle differentiation and Ca²⁺ homeostasis of muscle fibers. Dysregulation or lack of certain TRP channels can cause muscle diseases in genetically modified mice. Further, it has been suggested that abnormal function of TRP channels contributes to muscle fiber degeneration in Duchenne muscular dystrophy (DMD). In a recent study we showed that TRPC3 and C6, TRPV4, TRPM4 and TRPM7 are highly expressed in normal and mdx skeletal muscle, an animal model for DMD (Krüger et al. Neuromuscul. Disord. 18:501, 2008).

Methods: 

To investigate whether human muscle expresses the same TRP channel subset we applied RT-PCR and Western Blot analysis on human muscle biopsies and cultured human muscle cells. Transcripts coding for RyR1 and the voltage gated sodium channel served as controls and differentiation markers.

Results: 

In adult human muscle (n=5) TRPC1, TRPV2, V3 and TRPM7 were the most abundant isoforms and reached relative levels of 0.1 (TRPC1), 0.1 (TRPV2 and 3) and 0.4 (TRPM7); data given in relation to that of 18S rRNA (x 1.000.000). In proliferating cultured muscle cells (myoblasts) TRPC1, TRPV2 and TRPM7 were as well the most abundant TRP channel transcripts (n = 8–10). Interestingly, two days after differentiation start, the expression of TRPC1 and TRPC3, TRPV2-4, TRPM4 and M7 increased markedly and diminished during further differentiation to almost initial levels. Western Blot analyses of TRPC1 and TRPV2 proteins were widely in agreement with the RT-PCR data. However, in contrast to differentiating cells both proteins were hardly detectable in myoblasts.

Conclusions: 

We showed that TRP channels are expressed in both, cultured muscle cells and adult human skeletal muscle. However, they occur in a different pattern than in mouse skeletal muscle. This finding may have important impact for the presumed roles of TRP channels in muscle differentiation and for the process of fiber degeneration in Duchenne muscular dystrophy.