Abstract
The inhibition of the aberrant differentiation of tendon-derived stem cells (TDSCs) is a major target for the regeneration of damaged tendon tissues, as tendinopathy can be caused by the aberrant differentiation of TDSCs. We investigated whether the possible aberrant differentiation of TDSCs can be prevented by using adequate inhibitors. TDSCs extracted from chemically induced tendinopathy and injury-with-overuse tendinopathy models were cultured with 18α-glycyrrhetinic acid (AGA) and T0070907 to block osteogenic differentiation and adipogenic differentiation, respectively. The optimal dose of AGA decreased the osteogenic-specific marker Runx2 (Runt-related transcription factor 2), and T0070907 blocked the adipogenic-specific marker peroxisome proliferator-activated receptor gamma (PPARγ) in mRNA levels. We also found that AGA induced tenogenic differentiation in mRNA levels. However, T0070907 did not affect the tenogenic differentiation and regenerative capacity of TDSCs. We expect that optimal doses of AGA and T0070907 can prevent tendinopathy by inhibiting osteogenic and adipogenic differentiation, respectively. In addition, AGA and T0070907 may play important roles in the treatment of tendinopathy.
Highlights
Degenerative tendinopathy is a pathologic change in tendon tissues caused by repetitive traumatic injury and characterized by the formation of non-tendinous tissues in the tendon matrix [1]
In a search for the optimal doses of inhibitors for Runx2 and PPARγ, tendon-derived stem cells (TDSCs) were cultured with inhibitors of various concentrations (0, 1, 10, 25, 50, 100 μM) for 5 days
We used 10 μM of T0070907 as the cytotoxic dose killing under 50% of TDSCs extracted from the injury-with-overuse tendinopathy model (Figure 1C,D)
Summary
Degenerative tendinopathy is a pathologic change in tendon tissues caused by repetitive traumatic injury and characterized by the formation of non-tendinous tissues in the tendon matrix [1]. From histopathology in degenerative tendinopathy, calcifications, fibrocartilaginous or osseous metaplasia, and fatty degeneration can be found in addition to the deposition of mucoid material [2]. These abnormal non-tendinous tissues in the tendon contribute to widespread inferior biomechanics in the tendon [3], rendering the patients with tendinopathy physically disabled. The aberrant chondrogenic or adipogenic differentiation of TDSCs is related to the development of tendinopathy [4,5]. Chondrogenic differentiation was induced by kartogenin application [4], adipogenic differentiation after tendon injury, and osteogenic differentiation by chemical stress [5]
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