Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (low gravity)
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Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (low gravity)
Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight
Se-Jin Lee, Adam Lehar, Jessica U. Meir, Christina Koch, Andrew Morgan, Lara E. Warren, Renata Rydzik, View ORCID ProfileDaniel W. Youngstrom, Harshpreet Chandok, Joshy George, Joseph Gogain, Michael Michaud, Thomas A. Stoklasek, Yewei Liu, and View ORCID ProfileEmily L. Germain-Lee
PNAS September 22, 2020 117 (38) 23942-23951; first published September 8, 2020;
https://doi.org/10.1073/pnas.2014716117
Contributed by Se-Jin Lee, August 4, 2020 (sent for review July 14, 2020; reviewed by Shalender Bhasin and Paul Gregorevic)
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Significance
Among the major health challenges for astronauts during prolonged space travel are loss of muscle mass and loss of bone mass. Here, we investigated the effects of targeting the signaling pathway mediated by the secreted signaling molecules, myostatin and activin A, in mice sent to the International Space Station. We show that targeting this signaling pathway has significant beneficial effects in protecting against both muscle and bone loss in microgravity, suggesting that this strategy may be effective in preventing or treating muscle and bone loss not only in astronauts on prolonged missions but also in people with disuse atrophy on Earth, such as in older adults or in individuals who are bedridden or wheelchair-bound from illness.
Abstract
Among the physiological consequences of extended spaceflight are loss of skeletal muscle and bone mass. One signaling pathway that plays an important role in maintaining muscle and bone homeostasis is that regulated by the secreted signaling proteins, myostatin (MSTN) and activin A. Here, we used both genetic and pharmacological approaches to investigate the effect of targeting MSTN/activin A signaling in mice that were sent to the International Space Station. Wild type mice lost significant muscle and bone mass during the 33 d spent in microgravity. Muscle weights of Mstn −/− mice, which are about twice those of wild type mice, were largely maintained during spaceflight. Systemic inhibition of MSTN/activin A signaling using a soluble form of the activin type IIB receptor (ACVR2B), which can bind each of these ligands, led to dramatic increases in both muscle and bone mass, with effects being comparable in ground and flight mice. Exposure to microgravity and treatment with the soluble receptor each led to alterations in numerous signaling pathways, which were reflected in changes in levels of key signaling components in the blood as well as their RNA expression levels in muscle and bone. These findings have implications for therapeutic strategies to combat the concomitant muscle and bone loss occurring in people afflicted with disuse atrophy on Earth as well as in astronauts in space, especially during prolonged missions.
Se-Jin Lee, Adam Lehar, Jessica U. Meir, Christina Koch, Andrew Morgan, Lara E. Warren, Renata Rydzik, View ORCID ProfileDaniel W. Youngstrom, Harshpreet Chandok, Joshy George, Joseph Gogain, Michael Michaud, Thomas A. Stoklasek, Yewei Liu, and View ORCID ProfileEmily L. Germain-Lee
PNAS September 22, 2020 117 (38) 23942-23951; first published September 8, 2020;
https://doi.org/10.1073/pnas.2014716117
Contributed by Se-Jin Lee, August 4, 2020 (sent for review July 14, 2020; reviewed by Shalender Bhasin and Paul Gregorevic)
Article Figures & SI Info & Metrics
Significance
Among the major health challenges for astronauts during prolonged space travel are loss of muscle mass and loss of bone mass. Here, we investigated the effects of targeting the signaling pathway mediated by the secreted signaling molecules, myostatin and activin A, in mice sent to the International Space Station. We show that targeting this signaling pathway has significant beneficial effects in protecting against both muscle and bone loss in microgravity, suggesting that this strategy may be effective in preventing or treating muscle and bone loss not only in astronauts on prolonged missions but also in people with disuse atrophy on Earth, such as in older adults or in individuals who are bedridden or wheelchair-bound from illness.
Abstract
Among the physiological consequences of extended spaceflight are loss of skeletal muscle and bone mass. One signaling pathway that plays an important role in maintaining muscle and bone homeostasis is that regulated by the secreted signaling proteins, myostatin (MSTN) and activin A. Here, we used both genetic and pharmacological approaches to investigate the effect of targeting MSTN/activin A signaling in mice that were sent to the International Space Station. Wild type mice lost significant muscle and bone mass during the 33 d spent in microgravity. Muscle weights of Mstn −/− mice, which are about twice those of wild type mice, were largely maintained during spaceflight. Systemic inhibition of MSTN/activin A signaling using a soluble form of the activin type IIB receptor (ACVR2B), which can bind each of these ligands, led to dramatic increases in both muscle and bone mass, with effects being comparable in ground and flight mice. Exposure to microgravity and treatment with the soluble receptor each led to alterations in numerous signaling pathways, which were reflected in changes in levels of key signaling components in the blood as well as their RNA expression levels in muscle and bone. These findings have implications for therapeutic strategies to combat the concomitant muscle and bone loss occurring in people afflicted with disuse atrophy on Earth as well as in astronauts in space, especially during prolonged missions.
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