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

LDL-activated p38 in endothelial cells is mediated by Ras.

Y Zhu1, H Liao, N Wang

  • 1Division of Biomedical Sciences, University of California, Riverside, CA 92521, USA. yi.zhu@ucr.edu

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 14, 2001
PubMed
Summary
This summary is machine-generated.

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

Search for Light Pseudoscalar Bosons, Pair-Produced in Higgs Boson Decays in the Four-Electron Final State in Proton-Proton Collisions at sqrt[s]=13  TeV.

Physical review letters·2026
Same author

First Evidence for Mixing-Induced CP Violation in B_{s}^{0}→J/ψϕ(1020) Decays in pp Collisions at sqrt[s]=13  TeV.

Physical review letters·2026
Same author

Observation of Suppressed Charged-Particle Production in Ultrarelativistic Oxygen-Oxygen Collisions.

Physical review letters·2026
Same author

Measurement of D^{0} Meson Photoproduction in Ultraperipheral Heavy Ion Collisions.

Physical review letters·2026
Same author

Observation of tWZ Production at the CMS Experiment.

Physical review letters·2026
Same author

First Exclusive Reconstruction of the B^{*+}, B^{*0}, and B_{s}^{*0} Mesons and Precise Measurement of Their Masses.

Physical review letters·2026

Low-density lipoprotein (LDL) activates endothelial cells via the Ras-mediated p38 and JNK signaling pathways. This activation influences gene expression, contributing to endothelial dysfunction and atherosclerosis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cardiovascular Research

Background:

  • Endothelial dysfunction is a key factor in atherosclerosis.
  • Low-density lipoprotein (LDL) triggers inflammatory responses in endothelial cells (ECs).
  • Previous research indicated LDL activates c-Jun and AP-1 in ECs.

Purpose of the Study:

  • To investigate the activation of the p38-ATF-2 pathway by LDL in human ECs.
  • To elucidate the upstream mechanisms, specifically the role of Ras, in LDL-induced p38 activation.
  • To determine the role of p38 signaling in LDL-induced gene expression, such as E-selectin.

Main Methods:

  • Incubation of human ECs with LDL at pathophysiological concentrations.
  • Assessment of p38-ATF-2 activation, including ATF-2 phosphorylation and transactivation.

Related Experiment Videos

  • Analysis of Ras translocation and its interaction with Raf-1.
  • Utilizing a dominant-negative Ras mutant (RasN17) to inhibit LDL-induced signaling.
  • Employing a p38 inhibitor to assess its effect on LDL-induced E-selectin expression.

    • Main Results:

    • LDL activates the p38-ATF-2 pathway in human ECs in a time- and dose-dependent manner.
    • LDL induces Ras translocation to the cell membrane, enhancing its binding to Raf-1.
    • Inhibition of Ras signaling attenuates LDL-induced phosphorylation of ATF-2 and c-Jun, as well as AP-1 activity.
    • A p38 inhibitor reduces LDL-induced E-selectin mRNA levels.

    Conclusions:

    • LDL activates both p38 and JNK signaling pathways in ECs through Ras activation.
    • These Ras-mediated signaling events are critical in LDL-induced endothelial activation.
    • The findings provide insights into the molecular mechanisms underlying LDL-driven endothelial dysfunction.