Related Experiment Video

Updated: May 12, 2026

Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface
10:47

Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface

Published on: February 21, 2011

33.9K

Cigarette smoke-exposed microparticles released from T lymphocytes contribute to autophagy and apoptosis dysfunction

Gang Chen1, Zhaoji Meng2, Pei Wang1

  • 1Department of Respiratory and Critical Care Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Molecular Immunology
|March 6, 2025
PubMed

Insights

Cigarette smoke releases microparticles from T lymphocytes that harm vascular endothelial cells. These T lymphocyte-derived microparticles (TLMPs) disrupt endothelial cell proliferation, apoptosis, and autophagy, contributing to smoking-related vascular diseases.

Area of Science:

  • Immunology
  • Cell Biology
  • Pulmonary Medicine

Background:

  • Cigarette smoke is known to impair vascular endothelium function.
  • The precise mechanisms underlying cigarette smoke-induced endothelial dysfunction remain unclear.
  • T lymphocyte-derived microparticles (TLMPs) are implicated in various diseases.

Purpose of the Study:

  • To investigate the role of TLMPs in cigarette smoke-induced vascular endothelial dysfunction.
  • To determine how cigarette smoke affects TLMP release from human lymphocytes.
  • To examine the impact of TLMPs on endothelial cell proliferation, apoptosis, and autophagy.

Main Methods:

  • Cultured human lymphocytes exposed to cigarette smoke.
  • Quantification of microparticle release.
  • Assays for endothelial cell proliferation, apoptosis, and autophagy.
  • Measurement of cytokine levels.
  • Analysis of oxidative stress and STAT3 phosphorylation.

Main Results:

  • Cigarette smoke significantly increased the release of microparticles from T lymphocytes.
  • TLMPs from smoke-exposed T lymphocytes reduced endothelial proliferation.
  • TLMPs promoted endothelial cell apoptosis and autophagy.
  • Proinflammatory cytokine expression was elevated by TLMPs.
  • Mechanisms may involve oxidative stress and STAT3 signaling.

Conclusions:

  • Cigarette smoke promotes the release of TLMPs.
  • TLMPs contribute to endothelial cell apoptosis and autophagy dysfunction.
  • These findings elucidate a mechanism for cigarette smoke-related vascular damage.
Keywords:
ApoptosisAutophagyEndothelial cellsT lymphocyte-derived microparticlescigarette smoke

More Related Videos

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice10:37

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

13.2K
Generation of Lymphocytic Microparticles and Detection of their Proapoptotic Effect on Airway Epithelial Cells09:26

Generation of Lymphocytic Microparticles and Detection of their Proapoptotic Effect on Airway Epithelial Cells

Published on: February 20, 2015

8.9K

Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
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
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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...