LncRNA H19 Regulates Lipopolysaccharide (LPS)-Induced Apoptosis and Inflammation of BV2 Microglia Cells Through Targetin
- PDF / 3,388,826 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 35 Downloads / 200 Views
LncRNA H19 Regulates Lipopolysaccharide (LPS)‑Induced Apoptosis and Inflammation of BV2 Microglia Cells Through Targeting miR‑325‑3p/NEUROD4 Axis Enyi Gu1 · Weikun Pan1 · Kangyao Chen1 · Zhong Zheng1 · Guoling Chen1 · Pengde Cai1 Received: 5 August 2020 / Accepted: 2 November 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Spinal cord injury (SCI) is a devastating traumatic event worldwide. Work from the past decade has highlighted the key involvement of long non-coding RNAs (lncRNAs) in SCI. Nevertheless, the molecular action of lncRNA H19 in SCI is still not fully understood. The levels of H19, microRNA (miR)-325-3p, and neuronal differentiation 4 (NEUROD4) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Flow cytometry was performed to assess cell apoptosis. The levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and IL-6 were detected using the enzyme-linked immunosorbent assay (ELISA). Targeted relationships among H19, miR-325-3p, and NEUROD4 were confirmed by dual-luciferase reporter, RNA immunoprecipitation (RIP), or RNA pull-down assays. Our data showed that H19 level was overexpressed in lipopolysaccharide (LPS)-treated BV2 cells. H19 silencing alleviated LPS-evoked cell apoptosis and inflammation. Mechanistically, H19 in BV2 cells directly targeted miR-325-3p, and NEUROD4 was a direct target of miR-325-3p. Moreover, miR-325-3p was a functional target of H19 in regulating cell apoptosis and inflammation induced by LPS. Enforced expression of miR-325-3p relieved LPS-evoked cell apoptosis and inflammation through reducing NEUROD4. Furthermore, H19 in BV2 cells regulated NEUROD4 expression through targeting miR-325-3p. Our results identified that the silencing of H19 attenuated LPS-evoked microglia cell apoptosis and inflammation after SCI at least partially through targeting the miR-325-3p/NEUROD4 axis, highlighting a novel approach for SCI management. Keywords SCI · H19 · miR-325-3p · NEUROD4 · Inflammation
Introduction Acute spinal cord injury (SCI) is a devastating neurological disorder with high disability and mortality, affecting about 180,000 new individuals annually throughout the world (Rogers and Todd 2016; Singh et al. 2014). Despite improved management, including prevention measures Highlights: (1) miR-325-3p was a functional target of H19 in regulating cell apoptosis and inflammation induced by LPS; (2) H19 regulated NEUROD4 expression through targeting miR325-3p; (3) H19 silencing attenuated LPS-evoked microglia cell apoptosis and inflammation by targeting the miR-325-3p/ NEUROD4 axis. * Pengde Cai [email protected] 1
Department of Orthopedics, Fuzhou Second Hospital Affiliated To Xiamen University, Cangshan District, 47 Shangteng Road, Fuzhou 350007, Fujian, China
and biological treatments, SCI is still a devastating disease (Shank et al. 2017). SCI is a complicated pathology, and activated microglia after SCI is widely considered as a neuroprotective or neurotoxic regulator by mediating
Data Loading...
