Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Integrated gut metagenomic and muscle proteomic analysis reveals the role of dietary fermented extruded brewers' spent grain in enhancing pork quality through the gut-muscle axis.

Journal of animal science and biotechnology·2026
Same author

Genetic Control of Gut Microbial Diversity Enhances Host Resistance to Pathogenic Infections in <i>C. elegans</i>.

Microorganisms·2026
Same author

Nutritional value evaluation of solid-state fermented sorghum fed to meat ducks and its effects on growth performance and intestinal development.

Poultry science·2026
Same author

Neuromedin U Receptor NMUR3 Regulates Autophagy, Thereby Enhancing Thermal Tolerance in <i>C. elegans</i>.

International journal of molecular sciences·2025
Same author

Structural Characteristics of Mitochondrial Genomes of Two Species of Mackerel and Phylogenetic Analysis of Scombridae Family.

Biomolecules·2025
Same author

Super-enhancer MYCNOS-SE promotes chemoresistance in small cell lung cancer by recruiting transcription factors CTCF and KLF15.

Oncogene·2024

Related Experiment Video

Updated: Jan 3, 2026

Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
09:04

Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies

Published on: April 22, 2017

9.4K

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
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
EDNRBMethylprednisoloneNeural progenitor cellsSpinal cord injury

More Related Videos

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE
09:24

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Published on: April 15, 2014

18.1K
Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
09:44

Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases

Published on: May 2, 2025

574

Related Experiment Videos

Last Updated: Jan 3, 2026

Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
09:04

Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies

Published on: April 22, 2017

9.4K
Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE
09:24

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Published on: April 15, 2014

18.1K
Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
09:44

Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases

Published on: May 2, 2025

574

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.