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

Author:

Shu Tao12,Li Jiachun1,Gu Juyuan3,Wu Liang4,Xie Peng5,Zhang Dongfeng4,Li Wen2,Wan Junming1,Zheng Xiaozuo3ORCID

Affiliation:

1. Department of Orthopaedics, The Seventh Affiliated Hospital of Sun Yat-Sen University , Shenzhen, Guangdong 518000 , People’s Republic of China

2. Department of Spine Surgery, The Key Laboratory of Advanced Interdisciplinary Studies Center, The First Affiliated Hospital of Guangzhou Medical University , Guangzhou, Guangdong 510120 , People’s Republic of China

3. Department of Orthopedics, Hebei Medical University Third Hospital , Shijiazhuang, Hebei 050051 , People’s Republic of China

4. Department of Orthopedics, South China Hospital, Health Science Center, Shenzhen University , Shenzhen 518116 , People’s Republic of China

5. Department of Nuclear Medicine, Hebei Medical University Third Hospital , Shijiazhuang, Hebei 050051 , People’s Republic of China

Abstract

Abstract 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.

Funder

Guangzhou Science and Technology Project of China

Natural Science Foundation of Hebei Province

Publisher

Oxford University Press (OUP)

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3