Related Experiment Video

Updated: Jan 22, 2026

Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension
07:41

Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension

Published on: March 17, 2022

3.4K

ICAM-1 promotes the abnormal endothelial cell phenotype in chronic thromboembolic pulmonary hypertension

Jennifer Arthur Ataam1, Olaf Mercier2, Lilia Lamrani3

  • 1Research and Innovation Unit; Department of Medicine, Stanford University, Stanford, California.

The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation
|July 21, 2019
PubMed

Insights

Intercellular adhesion molecule-1 (ICAM-1) overexpression in pulmonary endothelial cells drives abnormal growth and survival in Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Inhibiting ICAM-1 normalizes these cellular changes, highlighting its therapeutic potential.

Area of Science:

  • Vascular Biology
  • Pulmonary Hypertension Pathophysiology
  • Cellular Signaling

Background:

  • Pulmonary endothelial cells are implicated in Chronic Thromboembolic Pulmonary Hypertension (CTEPH) pathogenesis.
  • Increased intercellular adhesion molecule-1 (ICAM-1) in CTEPH pulmonary endothelial cells suggests a key role.

Purpose of the Study:

  • To investigate the role of ICAM-1 in the abnormal phenotype of pulmonary endothelial cells in CTEPH.
  • To explore the mechanisms by which ICAM-1 influences endothelial cell behavior in CTEPH.

Main Methods:

  • Analysis of pulmonary endarterectomy specimens from CTEPH patients and control pulmonary artery specimens.
  • In vitro studies of isolated endothelial cells to assess ICAM-1 overexpression, growth, and apoptosis resistance.
  • Pharmacological inhibition of ICAM-1 and analysis of downstream signaling pathways (SRC, p38, ERK1/2) and survivin levels.

Main Results:

  • ICAM-1 was overexpressed in CTEPH endothelial cells, correlating with increased growth and apoptosis resistance.
  • Pharmacological inhibition of ICAM-1 reversed these abnormal cellular phenotypes.
  • ICAM-1 overexpression activates SRC, p38, and ERK1/2, leading to survivin overproduction and maintaining the abnormal endothelial cell phenotype.

Conclusions:

  • ICAM-1 plays a critical role in maintaining the abnormal endothelial cell phenotype observed in CTEPH.
  • Targeting ICAM-1 may offer a therapeutic strategy for managing CTEPH.
Abstract

Keywords:
Adhesion moleculesChronic thrombo-embolic hypertensionEndothelial dysfunctionICAM-1Survival signalling pathway

More Related Videos

Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet09:22

Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet

Published on: November 4, 2015

12.6K
Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis07:11

Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis

Published on: May 23, 2025

880

Related Concept Videos

Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
591
Chronic Obstructive Pulmonary Disease01:22

Chronic Obstructive Pulmonary Disease

COPD is defined as a heterogeneous lung condition marked by persistent respiratory symptoms such as dyspnea, cough, and sputum production, caused by abnormalities in the airways that cause airflow obstruction.
Smoking is a primary risk factor for COPD, with over 80% of patients having a history of it. Patients typically experience progressive dyspnea or labored breathing, frequent coughing, and recurrent pulmonary infections. Many eventually succumb to respiratory failure, characterized by...
2.3K
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors01:28

Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors

Phosphodiesterase 5 (PDE5) inhibitors are potent enzymes that function to hydrolyze cyclic nucleotides to their corresponding 5' monophosphates. Their unique biochemical properties have been applied in treating Pulmonary Arterial Hypertension (PAH).
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
577
Chronic Obstructive Pulmonary Disease-I: Introduction01:20

Chronic Obstructive Pulmonary Disease-I: Introduction

Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting respiratory condition requiring continuous attention and care. It is a progressive lung disease that leads to breathing challenges due to airflow obstruction. It manifests as persistent respiratory symptoms and restricted airflow resulting from abnormalities in the airways and alveoli, usually due to long-term exposure to harmful particles or gases. COPD mainly consists of two primary conditions: emphysema and chronic bronchitis.
3.6K
Chronic Obstructive Pulmonary Disease-V: Management01:29

Chronic Obstructive Pulmonary Disease-V: Management

Managing Chronic Obstructive Pulmonary Disease (COPD) involves a multifaceted approach to reduce symptoms, prevent exacerbations, improve overall health status, and slow disease progression. Key strategies include lifestyle modifications, pharmacotherapy, supportive therapies, and, in some cases, surgery. Here is an overview of the primary COPD management strategies:
Smoking Cessation
3.1K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
4.3K