These BMPs were reported to promote osteogenic, chondrogenic and adipogenic differentiation of mesenchymal stem cells (MSCs) including tendon-derived stem cells (TDSCs) isolated from healthy tendons in vitro. Įctopic expression of BMP-2, -4 and -7 were observed in clinical samples of tendinopathy and collagenase-induced (CI) tendon injury rat model which showed failed healing and ectopic chondro-ossification in tendons. Therefore, failed healing, rather than degeneration, is suggested as the pathogenesis of tendinopathy. The cells isolated from the tendinopathic tissue showed high metabolic activity. As a result, only symptomatic treatments are currently provided with limited success. The pathogenesis of tendinopathy remains unclear. Tissue metaplasia, with the presence of chondrocyte phenotype and occasional fatty and bony deposits, is observed. Histopathologically, tendinopathy is characterized by an increase of cellularity, vascularity, glycosaminoglycan deposition and loss of matrix organization. Tendinopathy is a chronic painful tendon disorder that is common among athletes and middle-aged people with repetitive tendon overuse. It also provided further support of BMPs and the BMP/Smad signaling pathway in the pathogenesis of tendinopathy. The sensitization of the BMP/Smad pathway in TDSCs (CI) might account for their higher non-tenogenic differentiation potential and hence altered fate. TDSCs (CI) exhibited higher total and phosphorylated Smad1/5/8 upon BMP-2 stimulation. TDSCs (CI) showed higher basal expression of total Smad1/5/8 but similar basal level of phosphorylated Smad1/5/8 compared to TDSCs (HT). ResultsĮxcept for the mRNA levels of Bmp7 and Bmpr2, there were significant higher mRNA and protein expression of BMPs and BMP receptors in TDSCs (CI) compared to TDSCs (HT). TDSCs from both sources were treated with rhBMP-2 and the expression of phosphorylated and total Smad1/5/8 was examined. The mRNA and protein expression of BMPs and BMP receptors in TDSCs (CI) and TDSCs (HT) were analysed. TDSCs (CI) and TDSCs (HT) were then isolated from the patellar tendon. MethodsĬollagenase or saline was injected into the patellar tendon of rats for 2 weeks. This study aimed to compare the activation state of the BMP/Smad pathway at basal level and upon BMP-2 stimulation in TDSCs (CI) and TDSCs (HT). We hypothesized that sensitization of the BMP/Smad pathway in TDSCs (CI) might account for this difference. TDSCs isolated from the CI model showed increased non-tenogenic differentiation potential and hence altered fate compared to the TDSCs isolated from the healthy animals (HT) but the mechanism is unclear. Ectopic expression of BMP-2, BMP-4 and BMP-7 was observed in clinical samples of tendinopathy and collagenase-induced (CI) tendon injury rat model.
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