LncRNA Neat1 Promotes Regeneration after Spinal Cord Injury by Targeting miR-29b
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LncRNA Neat1 Promotes Regeneration after Spinal Cord Injury by Targeting miR‑29b Guangtao Bai1 · Liang Jiang2 · Pingping Meng1 · Jiang Li1 · Chao Han1 · Yuyang Wang1 · Qiang Wang1 Received: 25 May 2020 / Accepted: 21 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Previous studies have shown that lncRNA NEAT1 and miR-29b are closely associated with repair of the injured spinal cord. However, the mechanism by which lncRNA NEAT1 promotes regeneration after spinal cord injury by regulating miR-29b has not been reported. To explore this mechanism, we established a rat model of spinal cord injury (SCI). The experimental rats were randomly assigned to one of six groups: the sham, model, si-NEAT1, miR-29b, si-NEAT1 + negative control and si-NEAT1 + si-miR-29b groups. The hind limb motor function of the rats was evaluated on days 1, 3, 7, 14, and 21 after modelling using the BBB rating scale. Seven days after the operation, attenuation of pathological changes in injured spinal cord tissues was evaluated by HE staining. Anterior horn neurons and cavities in the injured area were counted by Nissl staining. In addition, the TUNEL assay was employed to study neuronal apoptosis in the anterior horn, and the expression of the apoptotic proteins Bcl-2 and Bax was analysed by western blotting. Finally, the protein expression of GFAP, NCAM, GAP43, and SCG10 was measured by immunohistochemistry and western blotting. BBB scores revealed that decreasing the level of NEAT1 improved the hind limb motor function of the rats by increasing miR-29b expression. H&E and Nissl staining showed that silencing NEAT1 attenuated lesions in the spinal cord and decreased the number of cavities in the injured spinal cord by upregulating miR-29b. Immunohistochemistry and western blotting suggested that silencing NEAT1 significantly downregulated GFAP expression and upregulated GAP43, SCG10 and NCAM expression by inducing overexpression of miR29b. The TUNEL assay and western blotting also showed that silencing NEAT1 attenuated neuronal apoptosis. Keywords LncRNA NEAT1 · miR-29b · SCI · Regeneration
Introduction Long non-coding RNAs (lncRNAs), defined as non-coding RNAs longer than 200 nt, have become a hot topic in research, as they have been proven to play an important role in many life processes, including dosage compensation effects, epigenetic regulation, and the cell cycle (Kung et al. 2013; Yao et al. 2019). Nuclear enriched abundant Guangtao Bai and Liang Jiang are contributed equally to this work * Qiang Wang [email protected] 1
Department of Rehabilitation Medicine, The Affiliated Hospital of Qingdao University, Shandong Province 266555 Qingdao, China
Department of Ear‑Nose‑Throat, Qingdao Women and Children Hospital, Shandong Province 266555 Qingdao, China
2
transcript 1 (NEAT1) is a lncRNA that can function as a microRNA (miRNA) sponge to suppress interactions between miRNAs and their target mRNAs. By shaping the structure of paraspeckles (Clemson et al. 2009), NEAT1 can affect the expre
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