Related Experiment Video

Updated: Jul 23, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
08:28

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

3.7K

H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and

Xuelin Zhang1, Yang Che1, Lin Mao1

  • 1State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.

Genomics
|July 16, 2023
PubMed

Insights

Histone variant H3.3B plays a key role in aortic dissection by affecting vascular smooth muscle cell (VSMC) function and inflammation. Modulating H3.3B levels impacts disease progression in mouse models.

Area of Science:

  • Cardiovascular Biology
  • Epigenetics
  • Molecular Medicine

Background:

  • Aortic dissection is a life-threatening cardiovascular condition.
  • Histone variants are crucial for genome regulation but their role in aortic dissection is unclear.

Purpose of the Study:

  • To investigate the role and mechanism of histone variant H3.3B in aortic dissection.

Main Methods:

  • RNA sequencing and ChIP sequencing were used to analyze gene expression and binding sites.
  • In vivo studies involved VSMC-specific H3f3b knockin and knockout mouse models.

Main Results:

  • H3f3b manipulation altered VSMC synthetic gene expression and inflammatory responses.
  • H3.3B directly regulated genes involved in extracellular matrix, VSMC phenotype, and inflammatory signaling pathways.
  • VSMC-specific H3f3b knockin worsened aortic dissection, while knockout protected against it.
  • H3.3B regulated Spp1 and Ccl2, promoting VSMC apoptosis and macrophage recruitment.

Conclusions:

  • Histone variant H3.3B is vital in VSMC phenotypic transition, medial VSMC loss, and vascular inflammation in aortic dissection.
  • H3.3B influences key pathways implicated in the pathogenesis of aortic dissection.

Keywords:
Aortic dissectionCell apoptosisH3.3Phenotypic transitionVascular inflammationVascular smooth muscle cells

More Related Videos

A Novel Stretching Platform for Applications in Cell and Tissue Mechanobiology16:46

A Novel Stretching Platform for Applications in Cell and Tissue Mechanobiology

Published on: June 3, 2014

11.8K
Using In Vivo and Tissue and Cell Explant Approaches to Study the Morphogenesis and Pathogenesis of the Embryonic and Perinatal Aorta10:57

Using In Vivo and Tissue and Cell Explant Approaches to Study the Morphogenesis and Pathogenesis of the Embryonic and Perinatal Aorta

Published on: September 12, 2017

8.5K

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.6K
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
1.5K
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
11
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
16
Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
26
Autoregulation of Blood Flow01:17

Autoregulation of Blood Flow

Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation....
2.4K