%0 Journal Article
%T ¦Â2-Adrenergic receptor (¦Â2-AR) agonist formoterol suppresses differentiation of L6 myogenic cells by blocking PI3K¨CAKT pathway
%A Eun-Ju Song
%A Hyerim Lee
%A Ji-Hyun Kim
%A Kyunghwan Kim
%A Myung-ju Oh
%A So-Hyeon Kim
%A Sun-Ju Yi
%J Archive of "Animal Cells and Systems".
%D 2019
%R 10.1080/19768354.2018.1561516
%X ¦Â2-Adrenergic receptor (¦Â2-AR) is implicated in muscle metabolic activities such as glycogen metabolism, glucose uptake, lipolysis and muscle growth. However, the functional role of ¦Â2-AR in the differentiation of skeletal muscle is largely unknown. Here, we examined the functional role of ¦Â2-AR in L6 myoblast differentiation using the long-term-acting ¦Â2-AR-specific agonist formoterol. We observed that formoterol treatment strongly suppressed L6 myoblast differentiation and the expression of myosin heavy chain (MHC) in a dose- and time-dependent manner. Showing that both long-acting agonist (formoterol) and short-acting agonist (terbutaline) inhibited the induction of MHC protein, whereas ¦Â2-AR antagonist (ICI-118,551) upregulated MHC expression, we clearly demonstrated that ¦Â2-AR is involved in L6 myoblast differentiation. Furthermore, our pharmacological inhibition study revealed that the PI3K¨CAKT pathway is the main signaling pathway for myotube formation. Formoterol inhibited the activation of PI3K¨CAKT signaling, but not that of ERK signaling. Moreover, formoterol selectively inhibited AKT activation by IGF-I, but not by insulin. Collectively, our findings reveal a previously undocumented role of ¦Â2-AR activation in modulating the differentiation of L6 myoblasts
%K L6 myoblasts
%K muscle differentiation
%K ¦Â2-adrenergic receptor (¦Â2-AR)
%K formoterol
%K AKT pathway
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394304/