Role of β-adrenergic signaling in masseter muscle

In skeletal muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the β-AR subtypes in skeletal muscle are not fully understood....

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Bibliographic Details
Published in:PloS one 2019-04, Vol.14 (4), p.e0215539-e0215539
Main Authors: Ito, Aiko, Ohnuki, Yoshiki, Suita, Kenji, Ishikawa, Misao, Mototani, Yasumasa, Shiozawa, Kouichi, Kawamura, Naoya, Yagisawa, Yuka, Nariyama, Megumi, Umeki, Daisuke, Nakamura, Yoshiki, Okumura, Satoshi
Format: Article
Language:English
Subjects:
Abnormalities
Adrenergic beta-2 Receptor Agonists - pharmacology
Adrenergic receptors
Agonists
AKT protein
Animals
Apoptosis
Biology and Life Sciences
Ca2+/calmodulin-dependent protein kinase II
Calcium-binding protein
Calmodulin
Cardiac muscle
Clenbuterol
Clenbuterol - pharmacology
Dentistry
Dobutamine - pharmacology
Extracellular signal-regulated kinase
Fibrosis
Heart
Homeostasis
Hypertrophy
Kinases
Male
MAP kinase
MAP Kinase Signaling System
Masseter Muscle
Medicine
Medicine and Health Sciences
Mice
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Muscles
Musculoskeletal system
Orthodontics
Pharmacology
Phosphorylation
Phosphorylation - drug effects
Physical Sciences
Physiology
Proteins
Pulmonary arteries
Rapamycin
Receptors, Adrenergic, beta-1 - metabolism
Receptors, Adrenergic, beta-2 - metabolism
Skeletal muscle
Stimulation
TOR protein
TOR Serine-Threonine Kinases - metabolism
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Summary:In skeletal muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the β-AR subtypes in skeletal muscle are not fully understood. Therefore, in this work, we compared the effects of chronic β1- or β2-AR activation with a specific β1-AR agonist, dobutamine (DOB), or a specific β2-AR agonist, clenbuterol (CB), on masseter and cardiac muscles in mice. In cardiac muscle, chronic β1-AR stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic β2-AR stimulation induced cardiac hypertrophy without histological abnormalities. In masseter muscle, however, chronic β1-AR stimulation did not induce muscle hypertrophy, but did induce fibrosis and apoptosis concomitantly with increased levels of p44/42 MAPK (ERK1/2) (Thr-202/Tyr-204), calmodulin kinase II (Thr-286) and mammalian target of rapamycin (mTOR) (Ser-2481) phosphorylation. On the other hand, chronic β2-AR stimulation in masseter muscle induced muscle hypertrophy without histological abnormalities, as in the case of cardiac muscle, concomitantly with phosphorylation of Akt (Ser-473) and mTOR (Ser-2448) and increased expression of microtubule-associated protein light chain 3-II, an autophagosome marker. These results suggest that the β1-AR pathway is deleterious and the β2-AR is protective in masseter muscle. These data should be helpful in developing pharmacological approaches for the treatment of skeletal muscle wasting and weakness.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0215539