Related Experiment Video

Updated: Sep 4, 2025

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
08:00

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

Published on: July 10, 2019

6.2K

Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis

Zhiwei Zhang1,2, Suling Ding1, Zhe Wang3

  • 1Institutes of Biomedical Sciences and Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Acta Pharmaceutica Sinica. B
|July 18, 2022
PubMed

Insights

Histidine decarboxylase (HDC) deficiency enhances neutrophil migration and harmful neutrophil extracellular trap (NET) production after heart injury. Histamine treatment mitigates these effects, offering potential therapeutic targets for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Neutrophils and their count are linked to coronary disease severity after myocardial infarction.
  • Histidine decarboxylase (HDC) influences reactive oxidative species (ROS) and myeloid cell differentiation.
  • The specific role of HDC in neutrophils post-myocardial infarction is not well understood.

Purpose of the Study:

  • To investigate the impact of Histidine decarboxylase (HDC) deficiency on neutrophil function and cardiac outcomes following myocardial infarction.
  • To elucidate the molecular mechanisms underlying HDC's regulation of neutrophil extracellular trap (NET) formation and its consequences.

Main Methods:

  • Utilized Hdc-deficient (Hdc-/-) mice to study neutrophil behavior in a myocardial infarction model.
  • Analyzed neutrophil recruitment, migration, adhesion, ROS production, and NETosis.
  • Investigated the role of protein arginine methyltransferase 1 (PRMT1), histamine receptor 1 (H1R), ATP synthesis, and SWI/SNF complex in HDC-mediated effects.
  • Administered histamine or MS023 (a PRMT1 inhibitor) and assessed cardiac function and fibrosis.

Main Results:

  • Hdc deficiency led to disordered neutrophil recruitment, reduced adhesion, enhanced migration, and increased ROS/NET production.
  • NETs from Hdc-/- neutrophils promoted cardiomyocyte death and cardiac fibroblast activity.
  • PRMT1 expression was elevated in Hdc-/- neutrophils and modulated by histamine, H1R, ATP, and SWI/SNF.
  • Histamine or MS023 treatment reduced ROS and NETs, improved cardiac function, and decreased fibrosis and plasma NETs.

Conclusions:

  • HDC plays a critical role in regulating neutrophil extracellular trap (NET) formation via a histamine-H1R-ATP-SWI/SNF-PRMT1-ROS signaling pathway.
  • This pathway influences cardiac injury and repair post-myocardial infarction.
  • HDC, histamine, and related signaling molecules represent potential biomarkers and therapeutic targets for cardiovascular diseases.

Keywords:
Asymmetric demethylation arginineHDCMyocardial infarctionNeutrophil extracellular trapPRMT1Transcriptomics

More Related Videos

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury07:23

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

6.2K
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.4K

Related Concept Videos

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
25
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...
43
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
23
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...
48