The rotator cuff was harvested from the sham and RCT groups on various days for reverse transcription-polymerase chain reaction analysis of Tnfa, Ngf, Il1b, and Cox2 expression.
For the in vitro study, tenocytes were enzymatically isolated and cultured from patients with rotator cuff tear and treated with or without interleukin 1β (IL-1β) and PRP.
To assess the effects of PRP on tenocytes from degenerative rotator cuff tears with the concomitant use of a corticosteroid in interleukin 1β (IL-1β)-induced tendinopathic conditions.
We observed that carriers of the rare allele of both studied variants of TGFB1, as well as their G/A (rs1800470/rs1800469) haplotype, were less susceptible to RCT (p < 0.05).
Our findings show differential expression of matrix extracellular genes and TGFB family members in the degeneration process involved in rotator cuff tears.
The present study aimed to enhance the healing of the tendon‑bone interface following rotator‑cuff tear repair by the interposition of hydroxyapatite (HA) encapsulated with transforming growth factor β1 (TGFβ1).
PDGFRβ<sup>+</sup> PDGFRα<sup>+</sup> cells directly contribute to fibrosis and fatty degeneration after massive rotator cuff tears in the mouse model.
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.
To investigate potential mechanisms for fatty infiltration other than adipogenic differentiation of muscle stem cells, we examined the role of FABP4 in muscle fatty infiltration in an RCT mouse model.