LncRNA AC108925 promotes osteoblast differentiation of tendon-derived stem cells by targeting miR-146a-3p

Tendinopathy is a chronic orthopedic injury with high incidence[1], [2], [3], [4]. Tendinopathy is mainly caused by degenerative changes of the tendon caused by long-term overuse of the tendon. Due to the poor repair ability of the tendon itself, the recovery period after injury is long, and even disability is caused[5]. At present, the etiology and pathological mechanism of tendinopathy have not been determined, and there is still a lack of effective treatment methods for tendinopathy. The study of tendinopathy at the molecular level is helpful to develop new treatment strategies[2], [6], [7].

Tendon-derived stem cells (TDSCs) were a group of stem cells[8], [9], [10]. Like other type of stem cells, TDSCs presents characteristics like self-renewal capability and pluripotency[11], [12], and adipogenic differentiation ability[9], [10], [13]. Moreover, it has been reported that TDSCs conduce to the ostosis in tendon diseases[14], [15], [16].

Long non-coding RNAs (LncRNAs) is a member of the non-coding RNA family, [17], [18]. researchers declared that LncRNAs modulate diverse biological events, including cell differentiation by modulating gene expression[19], [20], [21], [22]. Moreover, LncRNAs participate in pathogenesis of diverse diseases including bone disease[23], [24].

In this study, the role of LncRNA in tendinopathy was investigated. Sequencing analysis was performed to compare the expression profile of LncRNAs in tendon tissues of the tendinopathy and healthy groups. Further, the effect of LncRNA AC108925 on the differentiation of TDSCs were also examined. This study revealed the biological meaning of AC108925 in tendinopathy, knockdown of AC108925 inhibited the osteogenic differentiation of hTDSCs via regulating the miR-146a-3p levels. Targeting the AC108925/miR-146a-3p axis might be a latent way to treat tendinopathy.

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