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

Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

501
Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...
501
Inflammation01:38

Inflammation

52.5K
Overview
52.5K
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

7.3K
The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
7.3K
Abnormal Proliferation02:23

Abnormal Proliferation

4.4K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.4K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

7.2K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.2K
Master Transcription Regulators02:23

Master Transcription Regulators

6.9K
Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
6.9K

You might also read

Related Articles

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

Sort by
Same author

Macrophage EHD1 Promotes Inflammation and Stabilizes Sortilin to Accelerate Atherosclerosis.

Circulation research·2026
Same author

Is Self-Reported Morbidity Associated with Nutritional Status? A Community-Based Study Among Urban Slum Dwelling Adult Males in West Bengal, India.

Ecology of food and nutrition·2026
Same author

In memoriam: Richard O. Hynes.

The Journal of cell biology·2026
Same author

From Byproduct to Regulator: The Expanding Role of Lactate and Lactylation in Cardiovascular Physiology and Disease.

Biology·2026
Same author

Deletion of endothelial KLF4 as a model for preeclampsia.

bioRxiv : the preprint server for biology·2026
Same author

Phytochemicals in arthritis management: insight into pharmacodynamic potency with pharmacokinetic profile.

Inflammopharmacology·2026
Same journal

A human-specific genetic modifier reconfigures large-scale cortical network dynamics underlying behavioral performance.

bioRxiv : the preprint server for biology·2026
Same journal

<i>Staphylococcus aureus</i> uses a eukaryotic-like uridyltransferase to make UDP-GlcNAc for cell wall synthesis.

bioRxiv : the preprint server for biology·2026
Same journal

Dynamic redistribution of eIF4F controls cap-dependent translation initiation.

bioRxiv : the preprint server for biology·2026
Same journal

When does additional information improve accuracy of RNA secondary structure prediction?

bioRxiv : the preprint server for biology·2026
Same journal

Normative brain-state trajectories reveal deviation from healthy aging in Alzheimer's disease.

bioRxiv : the preprint server for biology·2026
Same journal

Noradrenergic infraslow rhythm during sleep is the critical link between heart-rate dynamics and memory consolidation.

bioRxiv : the preprint server for biology·2026
See all related articles

Related Experiment Video

Updated: Jun 4, 2025

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

10.0K

Polycomb Repressive Complex 2 promotes atherosclerotic plaque vulnerability.

Divyesh Joshi1, Raja Chakraborty1, Tejas Bhogale1

  • 1Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, School of Medicine, Yale University, New Haven, CT 06511, USA.

Biorxiv : the Preprint Server for Biology
|December 20, 2024
PubMed
Summary
This summary is machine-generated.

Polycomb Repressive Complex 2 (PRC2) drives vascular inflammation and atherosclerosis by suppressing Klf2/4. Inhibiting PRC2 with tazemetostat significantly reduced plaque progression and improved stability in mice, offering a potential ASCVD treatment.

Keywords:
NotchPRC2Polycombatherosclerosisfluid shear stressvascular inflammation

More Related Videos

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

37.1K
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

8.2K

Related Experiment Videos

Last Updated: Jun 4, 2025

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

10.0K
Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

37.1K
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

8.2K

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Epigenetics

Background:

  • Atherosclerotic cardiovascular disease (ASCVD) is a leading global cause of death, driven by endothelial inflammation.
  • Klf2 and Klf4 are anti-inflammatory transcription factors that counterbalance endothelial activation in ASCVD.
  • Targeting vascular inflammation is crucial for developing effective ASCVD treatments.

Purpose of the Study:

  • To identify key regulators of vascular inflammation and ASCVD progression.
  • To investigate the role of Polycomb Repressive Complex 2 (PRC2) in endothelial inflammation and ASCVD.
  • To evaluate the therapeutic potential of targeting PRC2 for ASCVD treatment.

Main Methods:

  • Bioinformatic analysis to identify PRC2 as a direct suppressor of Klf2/4 transcription.
  • Investigation of Notch signaling's role in reversing PRC2-mediated epigenetic modifications.
  • Assessment of PRC2 activity in human ASCVD endothelium.
  • Pharmacological inhibition of PRC2 using tazemetostat in a mouse model of established ASCVD.

Main Results:

  • PRC2 was identified as a potent suppressor of the anti-inflammatory transcription factors Klf2/4.
  • PRC2 activity was found to be elevated in human ASCVD endothelium.
  • Treatment with the PRC2 inhibitor tazemetostat reduced ASCVD plaque progression by 50% and improved plaque stability markers in mice.

Conclusions:

  • PRC2 is a critical determinant of vascular inflammation and a driver of ASCVD progression.
  • Targeting PRC2, for example with tazemetostat, represents a promising therapeutic strategy for ASCVD.
  • This study reveals a fundamental mechanism in vascular inflammation, suggesting potential treatments for ASCVD and other vascular inflammatory diseases.