![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
Preview |
PDF (Original Article)
- Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
7MB |
![[thumbnail of Supplementary Material]](https://edoc.mdc-berlin.de/style/images/fileicons/application_msword.png) |
MS Word (Supplementary Material)
4MB |
| Item Type: | Article |
|---|---|
| Title: | Muscle atrophy due to nerve damage is accompanied by elevated myofibrillar protein synthesis rates |
| Creators Name: | Langer, H.T., Senden, J.M.G., Gijsen, A.P., Kempa, S., van Loon, Luc J. C. and Spuler, S. |
| 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, Animals, Rats |
| Source: | Frontiers in Physiology |
| ISSN: | 1664-042X |
| Publisher: | Frontiers Media SA |
| Volume: | 9 |
| Page Range: | 1220 |
| Date: | 31 August 2018 |
| Official Publication: | https://doi.org/10.3389/fphys.2018.01220 |
| PubMed: | View item in PubMed |
Repository Staff Only: item control page
