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1 Pharmacology, Emory University, Atlanta, GA, USA; Graduate Program in Biochemistry, Cell and Developmental Biology, Emory University, Atlanta, GA, USA
2 Pharmacology, Emory University, Atlanta, GA, USA
* To whom correspondence should be addressed. E-mail: gpavlat{at}emory.edu.
Loss of muscle mass occurs with disease, injury, aging, and inactivity. Restoration of normal muscle mass depends upon myofiber growth, the regulation of which is incompletely understood. Cyclooxygenase (COX)-2 is one of two isoforms of COX that catalyzes the synthesis of prostaglandins, paracrine hormones that regulate diverse physiological and pathophysiological processes. Previously, we demonstrated that the COX-2 pathway regulates early stages of myofiber growth during muscle regeneration. However, whether the COX-2 pathway plays a common role in adult myofiber growth or functions specifically during muscle regeneration is unknown. Therefore, we examined the role of COX-2 during myofiber growth following atrophy in mice. Muscle atrophy was induced by hindlimb suspension (HS) for 2 weeks, followed by a reloading period, during which mice were treated with either the COX-2 inhibitor SC-236 (6 mg/kg/day) or vehicle. COX-2 protein was expressed and SC-236 attenuated myofiber growth during reloading in both soleus and plantaris muscles. Attenuated myofiber growth in the soleus was associated with both decreased myonuclear addition and decreased inflammation, whereas neither of these processes mediated the effects of SC-236 on plantaris growth. In addition, COX-2-/- satellite cells exhibited impaired activation/proliferation in vitro, suggesting direct regulation of muscle cell activity by COX-2. Together, these data suggest that the COX-2 pathway plays a common regulatory role during various types of muscle growth via multiple mechanisms.
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