Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-23425
Schmutz, S; Fuchs, T; Regenfelder, F; Steinmann, P; Zumstein, M; Fuchs, B (2009). Expression of atrophy mRNA relates to tendon tear size in supraspinatus muscle. Clinical Orthopaedics and Related Research, 467(2):457-464.
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Skeletal muscle atrophy and fatty infiltration develop after tendon tearing. The extent of atrophy serves as one prognostic factor for the outcome of surgical repair of rotator cuff tendon tears. We asked whether mRNA of genes involved in regulation of degradative processes leading to muscle atrophy, ie, FOXOs, MSTN, calpains, cathepsins, and transcripts of the ubiquitin-proteasome pathway, are overexpressed in the supraspinatus muscle in patients with and without rotator cuff tears. We evaluated biopsy specimens collected during surgery of 53 consecutive patients with different sizes of rotator cuff tendon tears and six without tears. The levels of corresponding gene transcripts in total RNA extracts were assessed by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Supraspinatus muscle atrophy was assessed by MRI. The area of muscle tissue (or atrophy), decreased (increased) with increasing tendon tear size. The transcripts of CAPN1, UBE2B, and UBE3A were upregulated more than twofold in massive rotator cuff tears as opposed to smaller tears or patients without tears. These atrophy gene products may be involved in cellular processes that impair functional recovery of affected muscles after surgical rotator cuff repair. However, the damaging effects of gene products in their respective proteolytic processes on muscle structures and proteins remains to be investigated.
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|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Balgrist University Hospital, Swiss Spinal Cord Injury Center|
|DDC:||610 Medicine & health|
|Deposited On:||28 Oct 2009 09:05|
|Last Modified:||27 Nov 2013 17:29|
|Additional Information:||The original publication is available at www.springerlink.com|
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