Author:
Zheng Hongyu,Wang Tingting,Li Xiangmin,He Wei,Gong Zhiqiang,Lou Zhenkai,Wang Bing,Li Xingguo
Abstract
Abstract
Background
Intervertebral disc degeneration (IDD) is characterized by the loss of nucleus pulposus cells (NPCs) and phenotypic abnormalities. Accumulating evidence suggests that long noncoding RNAs (lncRNAs) are involved in the pathogenesis of IDD. In this study, we aimed to investigate the functional effects of lncRNA MALAT1 on NPCs in IDD and the possible mechanism governing these effects.
Results
We validated the decreased expression of MALAT1 in the IDD tissues, which was associated with decreased Collagen II and Aggrecan expression. In vitro, overexpressed MALAT1 could attenuate the effect of IL-1β on NPC proliferation, apoptosis, and Aggrecan degradation. In vivo, MALAT1 overexpression attenuated the severity of disc degeneration in IDD model rats. Our molecular study further demonstrated that MALAT1 could sponge miR-503, modulate the expression of miR-503, and activate downstream MAPK signaling pathways. The effects of MALAT1 on NPCs were partially reversed/aggregated by miR-503 mimics/inhibitor treatment.
Conclusion
Our data suggested that the MALAT1-miR-503-MAPK pathway plays a critical role in NPCs, which may be a potential strategy for alleviating IDD.
Funder
National Natural Science Foundation of China
Applied Basic Research Fundation of Yunnan Provinc
Joint Project on Applied Basic Research Foundation of Yunnan Science and Technology Department-Kunming Medical University
Yunnan Health Science and Technology Project
Kunming Medical University young and middle-aged academic and technical talents fund
Kunming Health and Family Planning Commission Medical and Health Science and Technology Program - Reserve Talents
Scientific and Technological Innovation Team of Spinal Degenerative Diseases Research in Kunming Medical University
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Molecular Biology
Cited by
15 articles.
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