JNK regulates muscle remodeling via myostatin/SMAD inhibition

Sarah J. Lessard (), Tara L. MacDonald, Prerana Pathak, Myoung Sook Han, Vernon G. Coffey, Johann Edge, Donato A. Rivas, Michael F. Hirshman, Roger J. Davis and Laurie J. Goodyear
Additional contact information
Sarah J. Lessard: Joslin Diabetes Center
Tara L. MacDonald: Joslin Diabetes Center
Prerana Pathak: Joslin Diabetes Center
Myoung Sook Han: University of Massachusetts Medical School
Vernon G. Coffey: Bond University
Johann Edge: Massey University
Donato A. Rivas: Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University
Michael F. Hirshman: Joslin Diabetes Center
Roger J. Davis: University of Massachusetts Medical School
Laurie J. Goodyear: Joslin Diabetes Center

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Skeletal muscle has a remarkable plasticity to adapt and remodel in response to environmental cues, such as physical exercise. Endurance exercise stimulates improvements in muscle oxidative capacity, while resistance exercise induces muscle growth. Here we show that the c-Jun N-terminal kinase (JNK) is a molecular switch that when active, stimulates muscle fibers to grow, resulting in increased muscle mass. Conversely, when muscle JNK activation is suppressed, an alternative remodeling program is initiated, resulting in smaller, more oxidative muscle fibers, and enhanced aerobic fitness. When muscle is exposed to mechanical stress, JNK initiates muscle growth via phosphorylation of the transcription factor, SMAD2, at specific linker region residues leading to inhibition of the growth suppressor, myostatin. In human skeletal muscle, this JNK/SMAD signaling axis is activated by resistance exercise, but not endurance exercise. We conclude that JNK acts as a key mediator of muscle remodeling during exercise via regulation of myostatin/SMAD signaling.

Date: 2018
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DOI: 10.1038/s41467-018-05439-3

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