Abstract
BackgroundTendon stem/progenitor cells (TSPCs) play a vital role in tendon repair and regeneration. Previously we found more adipocytes accumulated in the patellar tendon injury sites in aging rats compared with the young ones, of which the mechanism is still unknown. Here, we want to identify whether erroneous differentiation of TSPCs by aging accounts for the adipocyte accumulation.MethodsTSPCs from young and aging rats were isolated and propagated. Both young and aging TSPCs were induced to differentiate into adipocytes, and Oil red O staining, quantitative real-time polymerase chain reaction (qRT-PCR), western-blot and immunofluorescent staining were used to evaluate the capability of TSPCs. RNA sequencing was utilized to screen out different genes and signaling pathways related to adipogenesis between young and aging TSPCs.ResultsThe Oil red O staining showed there were more adipocytes formed in young TSPCs. Besides, adipogenic markers perilipin, peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding proteins alpha (C/EBPα) and Fatty acid-binding protein 4 (FABP4) were elevated both at gene and protein level. PPARγ signaling pathway was selected as our target via RNA sequencing. After adding the signaling activators, Rosiglitazone maleate (RM), inhibited adipogenesis of aging TSCs was reversed.ConclusionsIn conclusion, aging inhibited adipogenesis of TSPCs by down‐regulating PPARγ signaling. It is not likely that the adipocyte accumulation in aging tendon during repair was due to the aging of TSPCs. This may provide new targets for curing aging tendon injuries or tendinopathies.
Highlights
Tendon stem/progenitor cells (TSPCs) play a vital role in tendon repair and regeneration
Higher senescence markers β‐galactosidase and p16ink4a were expressed in aging TSPCs It was reported in previous researches that aging TSPCs have a significantly higher p16 ink4a and β-galactosidase expression level [2, 14]
The adipogenic differentiation was inhibited in aging TSPCs In order to explore whether the accumulation of adipocytes in aging tendon was caused by the change of adipogenic ability of TSPCs during aging, we conducted adipogenic induction culture of TSPCs in vitro
Summary
Tendon stem/progenitor cells (TSPCs) play a vital role in tendon repair and regeneration. We found more adipocytes accumulated in the patellar tendon injury sites in aging rats compared with the young ones, of which the mechanism is still unknown. We found that there were more adipocytes gathered in the process of tendon repair in aging rats than in young rats, which impaired the effect of tendon regeneration and repair, but the specific mechanism has not been elucidated. RUI et al found that the heterogeneous differentiation of TSPCs after changes in mechanical and biological environment led to calcified tendon disease [12]; another study found that the presence of tenomodulin can prevent TSPCs from differentiating into adipocytes, inhibiting the accumulation of adipocytes in the early stage of tendon repair [13]
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