Related Experiment Video

Updated: May 11, 2026

Live Cell Imaging during Mechanical Stretch
07:42

Live Cell Imaging during Mechanical Stretch

Published on: August 19, 2015

Oxidative stress mediates the disruption of airway epithelial tight junctions through a TRPM2-PLCγ1-PKCα signaling

Rui Xu1, Qi Li, Xiang-Dong Zhou

  • 1Department of Respiratory Medicine, the Second Affiliated Hospital, Chongqing University of Medical Science, Chongqing 400010, China. zxd999@263.net.

International Journal of Molecular Sciences
|May 1, 2013
PubMed

Insights

Oxidative stress damages epithelial barriers in lung diseases by degrading key proteins like zonula occludens-1 and claudin-2. This process is mediated by specific signaling pathways involving TRPM2, PLCγ1, and PKCα.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Molecular Signaling

Background:

  • Oxidative stress is linked to lung inflammation and epithelial barrier dysfunction.
  • Epithelial tight junctions (TJs) are crucial for lung barrier integrity.
  • Previous research suggests a connection between oxidative stress and TJ attenuation.

Purpose of the Study:

  • To investigate the molecular mechanisms by which oxidative stress affects epithelial TJs in human bronchial epithelial cells.
  • To identify the specific signaling pathways involved in oxidative stress-induced TJ degradation.

Main Methods:

  • Utilized Human Bronchial Epithelial-16 (16HBE) cell line.
  • Examined the degradation of tight junction proteins, specifically zonula occludens-1 (ZO-1) and claudin-2.
  • Investigated the role of the transient receptor potential melastatin 2 (TRPM2) channel, phospholipase Cγ1 (PLCγ1), and protein kinase Cα (PKCα) signaling cascade.

Main Results:

  • Demonstrated degradation of ZO-1 and claudin-2 in 16HBE cells under conditions related to oxidative stress.
  • Showed that this degradation is highly dependent on the activation of the TRPM2 channel.
  • Confirmed the involvement of the PLCγ1 and PKCα signaling cascade in the observed TJ protein degradation.

Conclusions:

  • Oxidative stress contributes to pulmonary inflammatory diseases by compromising epithelial barrier function.
  • The TRPM2 channel, PLCγ1, and PKCα signaling pathway are key mediators of oxidative stress-induced tight junction disruption in bronchial epithelial cells.
  • Targeting these pathways may offer therapeutic strategies for lung inflammatory diseases.

More Related Videos

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS07:33

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS

Published on: December 21, 2011

Related Concept Videos

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
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.