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

Epigenetic Regulation01:46

Epigenetic Regulation

33.1K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
33.1K
Epigenetic Regulation01:37

Epigenetic Regulation

3.6K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.6K
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

9.1K
The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
9.1K
Abnormal Proliferation02:23

Abnormal Proliferation

5.0K
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...
5.0K

You might also read

Related Articles

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

Sort by
Same author

Regulatory effect of Chinese Baijiu on gut microbiota and host metabolism.

Food research international (Ottawa, Ont.)·2026
Same author

Improving Multivariate Time-Series Anomaly Detection in Industrial Sensor Networks Using Entropy-Based Feature Aggregation.

Entropy (Basel, Switzerland)·2026
Same author

Potential causes and significance of elevated blood ketone levels in patients with heart failure with preserved ejection fraction.

Frontiers in nutrition·2026
Same author

Role of peptidylarginine deiminase 2 in a murine model of traumatic brain injury.

The journal of trauma and acute care surgery·2026
Same author

The role of arachidonic acid metabolites in the subtype classification and pathogenesis of primary aldosteronism.

iScience·2026
Same author

TMPRSS2 is dispensable for lethal SARS-CoV-2 BA.5 infection in humanized hACE2 golden hamsters.

European journal of medical research·2026

Related Experiment Video

Updated: Dec 11, 2025

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application
06:53

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application

Published on: July 9, 2020

5.4K

Nullifying epigenetic writer DOT1L attenuates neointimal hyperplasia.

Yitao Huang1, Go Urabe1, Mengxue Zhang1

  • 1Department of Surgery, College of Medicine and Davis Heart and Lung Research Institute, Wexner Medical Center, The Ohio State University, Columbus, OH, 43210, USA; Department of Physiology & Cell Biology, College of Medicine and Davis Heart and Lung Research Institute, Wexner Medical Center, The Ohio State University, Columbus, OH, 43210, USA.

Atherosclerosis
|August 18, 2020
PubMed
Summary

Disruptor of telomeric silencing 1-like (DOT1L) is upregulated in vascular injury, driving neointimal hyperplasia. Inhibiting DOT1L significantly reduces this condition, suggesting it as a therapeutic target for occlusive vascular diseases.

Keywords:
DOT1LEpigenetic targetH3K79 methylationIn vivo silencingNeointimal hyperplasia

More Related Videos

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

6.7K
Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models
08:34

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

Published on: May 14, 2014

12.4K

Related Experiment Videos

Last Updated: Dec 11, 2025

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application
06:53

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application

Published on: July 9, 2020

5.4K
Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

6.7K
Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models
08:34

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

Published on: May 14, 2014

12.4K

Area of Science:

  • Cardiovascular Biology
  • Epigenetics
  • Vascular Medicine

Background:

  • Histone methyltransferases are emerging therapeutic targets.
  • DOT1L (disruptor of telomeric silencing 1-like) is the sole known H3K79 methylation writer.
  • DOT1L's role in cardiovascular disease, specifically neointimal hyperplasia (IH), is largely unexplored.

Purpose of the Study:

  • To investigate the role of DOT1L in neointimal hyperplasia (IH) following vascular injury.
  • To assess the therapeutic potential of targeting DOT1L in occlusive vascular conditions.

Main Methods:

  • Neointimal hyperplasia was induced in rat carotid arteries via balloon angioplasty.
  • DOT1L expression and H3K79 methylation levels were assessed using immunostaining.
  • DOT1L was silenced using shRNA-lentivirus and inhibited pharmacologically with EPZ5676.
  • Effects on IH, smooth muscle α-actin, and proliferation markers (PCNA, cyclin-D1) were evaluated in vivo and in vitro.

Main Results:

  • DOT1L and H3K79me2/me3 levels significantly increased in injured carotid arteries.
  • DOT1L silencing reduced DOT1L, H3K79me2, and IH by 54.5%, 37.1%, and 76.5%, respectively.
  • DOT1L inhibition with EPZ5676 decreased H3K79me2/me3 and IH by 56.1%, 58.6%, and 39.9%, respectively.
  • Both DOT1L silencing and inhibition increased smooth muscle α-actin and reduced proliferation markers in smooth muscle cells.

Conclusions:

  • DOT1L is upregulated in response to angioplasty-induced vascular injury.
  • Genetic silencing or pharmacological inhibition of DOT1L effectively diminishes neointimal hyperplasia.
  • DOT1L represents a promising therapeutic target for treating (re)stenotic vascular conditions.