LncRNA MALAT1 exhibits positive effects on nucleus pulposus cell biology in vivo and in vitro by sponging miR-503

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

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