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Muscle atrophy due to nerve damage is accompanied by elevated myofibrillar protein synthesis rates
Langer, Henning Senden, Joan M. Gijsen, Annemie P. Kempa, Stefan van Loon, Luc Spuler, Simone
Langer, Henning
Senden, Joan M.
Gijsen, Annemie P.
Kempa, Stefan
van Loon, Luc
Spuler, Simone
Abstract
Muscle loss is a severe complication of many medical conditions such as cancer, cardiac failure, muscular dystrophies, and nerve damage. The contribution of myofibrillar protein synthesis (MPS) to the loss of muscle mass after nerve damage is not clear. Using deuterium oxide (D2O) labeling, we demonstrate that MPS is significantly increased in rat m. tibialis anterior (TA) compared to control (3.23 ± 0.72 [damaged] to 2.09 ± 0.26%∗day−1 [control]) after 4 weeks of nerve constriction injury. This is the case despite substantial loss of mass of the TA (350 ± 96 mg [damaged] to 946 ± 361 mg [control]). We also show that expression of regulatory proteins involved with MPS (p70s6k1: 2.4 ± 0.3 AU [damaged] to 1.8 ± 0.2 AU [control]) and muscle protein breakdown (MPB) (MAFbx: 5.3 ± 1.2 AU [damaged] to 1.4 ± 0.4 AU [control]) are increased in nerve damaged muscle. Furthermore, the expression of p70s6k1 correlates with MPS rates (r2 = 0.57). In conclusion, this study shows that severe muscle wasting following nerve damage is accompanied by increased as opposed to decreased MPS.
Keywords
skeletal muscle, atrophy, muscle loss, myofibrillar, protein synthesis, nerve damage, stable isotope, deuterium oxide
Date
2018
Type
Journal article
Journal
Frontiers in Physiology
Book
Volume
9
Issue
1220
Page Range
1-10
Article Number
ACU Department
Centre for Exercise and Nutrition
Faculty of Health Sciences
Faculty of Health Sciences
Collections
Relation URI
Source URL
Event URL
Open Access Status
Open access
License
CC BY-NC 3.0
File Access
Open