Abstract
Fatty infiltration in muscle is often observed in patients with sizable rotator cuff tear (RCT) and is thought to be an irreversible event that significantly compromises muscle plasticity and contraction strength. These changes in the mechanical properties of the affected muscle render surgical repair of RCT highly formidable. Therefore, it is important to learn more about the pathology of fatty infiltration to prevent this undesired condition. In the present study, we aimed to generate a mouse model that can reliably recapitulate some of the important characteristics of muscular fatty infiltration after RCT in humans. We found that fatty infiltration can be efficiently induced by a combination of the following procedures: denervation of the suprascapular nerve, transection of the rotator cuff tendon, and resection of the humeral head. Using this model, we found that platelet-derived growth factor receptor-α (PDGFRα)-positive mesenchymal stem cells are induced after this intervention and that inhibition of PDGFR signaling by imatinib treatment can significantly suppress fatty infiltration. Taken together, the present study presents a reliable fatty infiltration mouse model and suggests a key role for PDGFRα-positive mesenchymal stem cells in the process of fatty infiltration after RCT in humans.
Highlights
That these cells could constitute a potential target in preventing fatty infiltration
Using this mouse model, we found that PDGFRα-positive cells are induced after massive Rotator cuff tear (RCT) and that pharmacological inhibition of PDGFR can significantly suppress the progression of fatty infiltration
The present study describes a reliable mouse model which can efficiently induce fatty infiltration in the SSP muscle in 4 weeks
Summary
That these cells could constitute a potential target in preventing fatty infiltration. This hypothesis has not been fully addressed. We describe a mouse model that can efficiently induce fatty infiltration in the suprascapular (SSP) muscle in 4 weeks. Using this mouse model, we found that PDGFRα-positive cells are induced after massive RCT and that pharmacological inhibition of PDGFR can significantly suppress the progression of fatty infiltration.
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