Persistent URL of this record https://hdl.handle.net/1887/97677
In Collections
This item can be found in the following collections:
Molecular signatures of age-associated chronic degeneration of shoulder muscles
mobility limitations, pain and frailty. The intrinsic molecular mechanisms are poorly
understood due to multifactorial causes, slow progression with age and variations
between individuals. Understanding the underlying molecular mechanisms could
lead to new treatment options which are currently limited. Shoulder complaints are
highly common in the elderly, and therefore, muscles of the shoulder’s rotator cuff
could be considered as a model for chronic age-associated muscle degeneration.
Diseased shoulder muscles were characterized by muscle atrophy and fatty infiltration
compared with unaffected shoulder muscles. We confirmed fatty infiltration using
histochemical analysis. Additionally, fibrosis and loss of contractile myosin expression
were found in diseased muscles. Most cellular features, including proliferation rate,
apoptosis and cell senescence,...Show moreChronic muscle diseases are highly prevalent in the elderly causing severe
mobility limitations, pain and frailty. The intrinsic molecular mechanisms are poorly
understood due to multifactorial causes, slow progression with age and variations
between individuals. Understanding the underlying molecular mechanisms could
lead to new treatment options which are currently limited. Shoulder complaints are
highly common in the elderly, and therefore, muscles of the shoulder’s rotator cuff
could be considered as a model for chronic age-associated muscle degeneration.
Diseased shoulder muscles were characterized by muscle atrophy and fatty infiltration
compared with unaffected shoulder muscles. We confirmed fatty infiltration using
histochemical analysis. Additionally, fibrosis and loss of contractile myosin expression
were found in diseased muscles. Most cellular features, including proliferation rate,
apoptosis and cell senescence, remained unchanged and genome-wide molecular
signatures were predominantly similar between diseased and intact muscles.
However, we found down-regulation of a small subset of muscle function genes,
and up-regulation of extracellular region genes. Myogenesis was defected in muscle
cell culture from diseased muscles but was restored by elevating MyoD levels. We
suggest that impaired muscle functionality in a specific environment of thickened
extra-cellular matrix is crucial for the development of chronic age-associated muscle
degeneration.Show less
- All authors
- Raz, Y.; Henseler, J.F.; Kolk, A.; Tatum, Z.; Groosjohan, N.K.; Verwey, N.E.; Arindrarto, W.; Kielbasa, S.M.; Nagels, J.; Hoen, P.A.C. 't; Nelissen, R.G.H.H.; Raz, V.
- Date
- 2016
- Journal
- Oncotarget
- Volume
- 23
- Issue
- 7
- Pages
- 8513 - 8523