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EDNRB Reverses Methylprednisolone-Mediated Decrease in Neural Progenitor Cell Viability via Regulating PI3K/Akt
Shiyuan Li1, Ming Zeng2, Lin Yang2
1Department of Spinal Surgery, the First People's Hospital of Foshan, North Lingnan Avenue 81, Foshan, 528000, Guangdong, China. 214265029@qq.com.
Journal of Molecular Neuroscience : MN
|November 25, 2019
Summary
Methylprednisolone (MP) inhibits neural progenitor cell (NPC) proliferation, but activating the endothelin receptor B (EDNRB) reverses this effect. This reversal is mediated by lncRNAs and the PI3K/AKT pathway, offering potential therapeutic strategies for spinal cord injury.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Spinal cord injury (SCI) involves complex cellular mechanisms affecting neural progenitor cells (NPCs).
- Methylprednisolone (MP) is a corticosteroid used in SCI treatment, but its precise effects on NPCs require further elucidation.
- Endothelin receptor B (EDNRB) signaling plays a role in cellular regulation and may interact with MP's effects.
Purpose of the Study:
- To investigate the mechanisms by which methylprednisolone (MP) affects neural progenitor cell (NPC) proliferation.
- To determine the role of endothelin receptor B (EDNRB) in mediating MP's effects on NPCs.
- To identify key molecular pathways and lncRNAs involved in MP and EDNRB-mediated regulation of NPCs in the context of spinal cord injury.
Main Methods:
- Primary NPCs were isolated and treated with MP and an EDNRB agonist (IRL-1620).
- Cell viability was assessed using MTS assays.
- RNA-sequencing (RNA-seq) was employed to identify differentially expressed lncRNAs, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.
- Protein expression of the PI3K/AKT pathway was analyzed via Western blotting, and lncRNA expression was examined after inhibiting the AKT pathway.
Main Results:
- MP treatment decreased NPC viability, an effect reversed by the EDNRB agonist.
- RNA-seq identified specific lncRNAs (NONRATT030699.2, NONRATT004088.2, NONRATT005601.2) potentially involved in MP and EDNRB signaling.
- The PI3K/AKT pathway was identified as a key mediator; EDNRB activation promoted NPC proliferation by activating PI3K/AKT, suppressing p-ERK, and increasing cyclin D1.
- Inhibition of the AKT pathway altered lncRNA expression, confirming its role in the observed effects.
Conclusions:
- Methylprednisolone inhibits neural progenitor cell proliferation.
- Activation of endothelin receptor B reverses the inhibitory effects of MP on NPCs.
- The reversal mechanism involves lncRNAs and the PI3K/AKT signaling pathway, suggesting a novel therapeutic avenue for spinal cord injury.
