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 Experiment Videos

Ceramide-induced apoptosis in cortical neurons is mediated by an increase in p38 phosphorylation and not by the

S Willaime1, P Vanhoutte, J Caboche

  • 1Laboratoire Signalisation Neuronale et Régulation Génique (FRE 2371), boîte 14, 9 quai Saint Bernard, 75005 Paris, France. sandrine.willaime@snv.jussieu.fr

The European Journal of Neuroscience
|June 26, 2001
PubMed
Summary

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

Challenges in the Development of Drugs for Sarcopenia and Frailty - Report from the International Conference on Frailty and Sarcopenia Research (ICFSR) Task Force.

The Journal of frailty & aging·2022
Same author

Testing the efficacy and safety of BIO101, for the prevention of respiratory deterioration, in patients with COVID-19 pneumonia (COVA study): a structured summary of a study protocol for a randomised controlled trial.

Trials·2021
Same author

Head down tilt 15° in experimental intracerebral hemorrhage: a randomized noninferiority safety trial.

European journal of neurology·2020
Same author

An unusual suspect for heart failure.

Acute medicine·2020
Same author

An unusual suspect for heart failure.

Acute medicine·2020
Same author

Neural circuit repair by low-intensity magnetic stimulation requires cellular magnetoreceptors and specific stimulation patterns.

Science advances·2019

C2-ceramide triggers neuronal apoptosis by modulating mitogen-activated protein kinase (MAPK) pathways. Specifically, p38 activation is crucial for ceramide-induced apoptosis in primary cortical neurons.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Ceramide is a key sphingomyelin pathway molecule involved in various cellular functions.
  • Ceramide acts as a second messenger regulating cell proliferation, differentiation, growth arrest, and apoptosis.

Purpose of the Study:

  • To investigate the role of c2-ceramide in inducing apoptosis in primary cortical neurons.
  • To elucidate the involvement of mitogen-activated protein kinase (MAPK) cascades in c2-ceramide-induced neuronal apoptosis.

Main Methods:

  • Primary cortical neuron cultures were treated with c2-ceramide.
  • Mitogen-activated protein kinase (MAPK) cascades, including ERK, p38, and JNK, were analyzed using immunoblotting.
  • The effects of specific MAPK inhibitors (PD98059 and SB203580) on apoptosis were assessed.

Related Experiment Videos

  • mRNA levels of c-jun, c-fos, and p53 were quantified.

    • Main Results:

    • C2-ceramide induced apoptosis in primary cortical neurons.
    • C2-ceramide decreased extracellular signal-regulated kinases (ERKs) and MAPK kinases (MEKs) phosphorylation.
    • C2-ceramide increased p38 and c-Jun N-terminal kinase (JNK) phosphorylation.
    • Inhibition of p38 partially protected neurons from apoptosis, indicating its necessity.
    • C2-ceramide increased c-jun, c-fos, and p53 mRNA levels independently of p38 activation.

    Conclusions:

    • The p38 MAPK pathway is essential for c2-ceramide-induced apoptosis in primary cortical neurons.
    • Differential modulation of MAPK cascades, particularly p38 activation, plays a critical role in ceramide-mediated neuronal cell death.
    • The study clarifies the temporal dynamics of MAPK and gene expression during ceramide-induced neuronal apoptosis.