Long noncoding RNA UCA1 promotes the chondrogenic differentiation of human bone marrow mesenchymal stem cells via regulating PARP1 ubiquitination

Bone marrow mesenchymal stem cells (BMSCs) possess the potential to differentiate into cartilage cells. Long noncoding RNA (lncRNAs) urothelial carcinoma associated 1 (UCA1) has been confirmed to improve the chondrogenic differentiation of marrow mesenchymal stem cells (MSCs). Herein, we further inv...

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Published in:Stem cells (Dayton, Ohio) Ohio), 2024-08, Vol.42 (8), p.752-762
Main Authors: Shu, Tao, Li, Jiachun, Gu, Juyuan, Wu, Liang, Xie, Peng, Zhang, Dongfeng, Li, Wen, Wan, Junming, Zheng, Xiaozuo
Format: Article
Language:English
Subjects:
Bone Marrow Cells - cytology
Bone Marrow Cells - metabolism
Cell Differentiation - genetics
Chondrogenesis - genetics
Humans
Mesenchymal Stem Cells - cytology
Mesenchymal Stem Cells - metabolism
NF-kappa B - metabolism
Poly (ADP-Ribose) Polymerase-1 - genetics
Poly (ADP-Ribose) Polymerase-1 - metabolism
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal Transduction
Ubiquitination
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Summary:Bone marrow mesenchymal stem cells (BMSCs) possess the potential to differentiate into cartilage cells. Long noncoding RNA (lncRNAs) urothelial carcinoma associated 1 (UCA1) has been confirmed to improve the chondrogenic differentiation of marrow mesenchymal stem cells (MSCs). Herein, we further investigated the effects and underlying mechanisms of these processes. The expression of UCA1 was positively associated with chondrogenic differentiation and the knockdown of UCA1 has been shown to attenuate the expression of chondrogenic markers. RNA pull-down assay and RNA immunoprecipitation showed that UCA1 could directly bind to PARP1 protein. UCA1 could improve PARP1 protein via facilitating USP9X-mediated PARP1 deubiquitination. Then these processes stimulated the NF-κB signaling pathway. In addition, PARP1 was declined in UCA1 knockdown cells, and silencing of PARP1 could diminish the increasing effects of UCA1 on the chondrogenic differentiation from MSCs and signaling pathway activation. Collectively, these outcomes suggest that UCA1 could act as a mediator of PARP1 protein ubiquitination and develop the chondrogenic differentiation of MSCs.
ISSN:1066-5099
1549-4918
1549-4918
DOI:10.1093/stmcls/sxae038