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

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

You might also read

Related Articles

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

Sort by
Same author

Beyond Reperfusion: Early Molecular Drivers and Therapeutic Opportunities in Acute Post-Infarction Cardiac Fibrosis.

International journal of molecular sciences·2026
Same author

Availability of Charged tRNAs Drives Maximal Protein Synthesis at Intermediate Levels of Codon Usage Bias.

Bulletin of mathematical biology·2026
Same author

Atherosclerotic Plaque Instability and Rupture: Recommended Mouse Models to Empower Clinically Relevant Discoveries, Diagnostics, and Therapeutics.

Arteriosclerosis, thrombosis, and vascular biology·2025
Same author

Availability of charged tRNAs drives maximal protein synthesis at intermediate levels of codon usage bias.

bioRxiv : the preprint server for biology·2025
Same author

Association of constipation with increased risk of hypertension and cardiovascular events in elderly Australian patients.

Scientific reports·2023
Same author

Proteasome inhibition reduces plasma cell and antibody secretion, but not angiotensin II-induced hypertension.

Frontiers in cardiovascular medicine·2023

Related Experiment Video

Updated: Jun 25, 2026

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

NKT cell subsets mediate differential proatherogenic effects in ApoE-/- mice.

Kelly To1, Alex Agrotis, Gurdyal Besra

  • 1Vascular Biology & Atherosclerosis Laboratory, Baker IDI Heart & Diabetes Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia. Kelly.To@bakeridi.edu.au

Arteriosclerosis, Thrombosis, and Vascular Biology
|March 3, 2009
PubMed
Summary

CD4+ NKT cells, not DN NKT cells, drive atherosclerosis development. Inhibitory Ly49 receptors on NKT cell subtypes regulate proatherogenic cytokine secretion, influencing lesion size in ApoE-/- mice.

More Related Videos

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Related Experiment Videos

Last Updated: Jun 25, 2026

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Area of Science:

  • Immunology
  • Cardiovascular Research
  • Atherosclerosis Pathogenesis

Background:

  • NKT cells contribute to atherosclerosis, but specific subtypes involved remain unclear.
  • ApoE-/- mice are a standard model for studying atherosclerosis.
  • Neonatal thymectomy (3dTx) can induce NKT cell deficiency.

Purpose of the Study:

  • Identify which NKT cell subtypes (CD4+ or DN NKT) promote atherogenesis.
  • Investigate the role of inhibitory Ly49 receptors in NKT cell-mediated atherosclerosis.

Main Methods:

  • Utilized ApoE-/- mice rendered NKT cell-deficient via neonatal thymectomy (3dTx).
  • Assessed atherosclerosis development on a high-fat diet with/without adoptive NKT cell transfer.
  • Analyzed NKT cell subtype homing, Ly49 receptor expression, and cytokine secretion in vitro.

Main Results:

  • Thymectomized mice showed significantly smaller atherosclerotic lesions, confirming NKT cell deficiency.
  • Adoptive transfer of CD4+ NKT cells, but not DN NKT cells, increased lesion size 2.5-fold.
  • DN NKT cells expressed higher inhibitory Ly49 receptors, impacting cytokine secretion differently based on MHC class I expression.

Conclusions:

  • CD4+ NKT cells are the primary drivers of NKT cell-mediated proatherogenic activity.
  • Differential expression of inhibitory Ly49 receptors by NKT cell subtypes regulates their proatherogenic function.