Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

348
Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
348
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.8K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.8K
Cystic Fibrosis: Management01:24

Cystic Fibrosis: Management

215
Cystic fibrosis (CF) is an autosomal recessive disorder that predominantly affects individuals of Northern European descent, occurring at a rate of 1 in 3500. It is caused by a genetic mutation in a gene on chromosome 7, most commonly the ΔF508 mutation, that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This results in thicker mucus secretions and obstruction pathologies in multiple organs, including the lungs and sinuses.
Sinus disease and chronic...
215

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Assessment of occupational exposure to engineered nanomaterials in research laboratories using personal monitors.

The Science of the total environment·2018
Same author

Effects of Combined Aerobic-Strength Training vs Fitness Education Program in COPD Patients.

International journal of sports medicine·2017
Same author

Teaching Neuro<i>Images</i>: Figure of 8: The clue to the diagnosis of AMPD2 pontocerebellar hypoplasia (PCH9).

Neurology·2017
Same author

The effects of mild germinal matrix-intraventricular haemorrhage on the developmental white matter microstructure of preterm neonates: a DTI study.

European radiology·2017
Same author

Added value of diffusion weighted imaging in pediatric central nervous system embryonal tumors surveillance.

Oncotarget·2017
Same author

Concomitant mitral regurgitation and aortic stenosis: one step further to low-flow preserved ejection fraction aortic stenosis.

European heart journal. Cardiovascular Imaging·2017

Related Experiment Video

Updated: Aug 31, 2025

Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke
09:50

Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke

Published on: February 12, 2015

11.3K

Carbon nanoparticles adversely affect CFTR expression and toxicologically relevant pathways.

Torben Stermann1, Thach Nguyen1, Burkhard Stahlmecke2

  • 1IUF - Leibniz-Research Institute for Environmental Medicine, Auf'm Hennekamp 50, 40225, Duesseldorf, Germany.

Scientific Reports
|August 22, 2022
PubMed
Summary
This summary is machine-generated.

Exposure to carbon nanoparticles (CNP) in air pollution significantly reduces cystic fibrosis transmembrane conductance regulator (CFTR) expression in lung cells. This reduction is linked to increased oxidative stress, apoptosis, and DNA damage, impacting respiratory health.

More Related Videos

A Fluorescence-Based Assay of Membrane Potential for High-Throughput Functional Study of Two Endogenous Ion Channels in Two Epithelial Cell Lines
06:59

A Fluorescence-Based Assay of Membrane Potential for High-Throughput Functional Study of Two Endogenous Ion Channels in Two Epithelial Cell Lines

Published on: June 22, 2022

2.2K
Nasal Potential Difference to Quantify Trans-epithelial Ion Transport in Mice
08:55

Nasal Potential Difference to Quantify Trans-epithelial Ion Transport in Mice

Published on: July 4, 2018

7.8K

Related Experiment Videos

Last Updated: Aug 31, 2025

Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke
09:50

Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke

Published on: February 12, 2015

11.3K
A Fluorescence-Based Assay of Membrane Potential for High-Throughput Functional Study of Two Endogenous Ion Channels in Two Epithelial Cell Lines
06:59

A Fluorescence-Based Assay of Membrane Potential for High-Throughput Functional Study of Two Endogenous Ion Channels in Two Epithelial Cell Lines

Published on: June 22, 2022

2.2K
Nasal Potential Difference to Quantify Trans-epithelial Ion Transport in Mice
08:55

Nasal Potential Difference to Quantify Trans-epithelial Ion Transport in Mice

Published on: July 4, 2018

7.8K

Area of Science:

  • Environmental Health
  • Cell Biology
  • Respiratory Medicine

Background:

  • Cystic fibrosis (CF) is a genetic disorder caused by CFTR gene mutations, leading to respiratory failure.
  • Ultrafine carbonaceous particles from air pollution are a growing health concern.
  • The impact of carbon nanoparticles (CNP) on CFTR expression in lung cells was previously unknown.

Purpose of the Study:

  • To investigate the effects of spark-ablated carbon nanoparticles (CNP) on CFTR expression in human bronchial epithelial cells.
  • To assess the cellular and molecular responses of lung cells to CNP exposure.

Main Methods:

  • Human bronchial epithelial cells (16HBE14o-) were cultured under air-liquid interface (ALI) conditions.
  • Cells were exposed to spark-ablated CNP for 4 hours.
  • CFTR expression, epithelial barrier integrity, and transcriptomic profiles were analyzed.

Main Results:

  • ALI-cultured cells showed good barrier integrity and elevated CFTR expression prior to exposure.
  • CNP exposure decreased epithelial barrier integrity and reduced both CFTR transcript and protein levels.
  • Transcriptomic analysis indicated that CNP exposure induced oxidative stress, apoptosis, and DNA damage.

Conclusions:

  • Spark-ablated carbon nanoparticles reduce CFTR expression in lung epithelial cells.
  • CNP exposure triggers cellular stress responses including oxidative stress, apoptosis, and DNA damage.
  • These findings highlight a potential mechanism by which air pollution exacerbates respiratory conditions like cystic fibrosis.