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 Experiment Videos

Cigarette smoke induces cellular senescence.

Toru Nyunoya1, Martha M Monick, Aloysius Klingelhutz

  • 1Division of Pulmonary, Critical Care, and Occupational Medicine, 100 EMRB, Iowa City, IA 52242, USA. toru-nyunoya@uiowa.edu

American Journal of Respiratory Cell and Molecular Biology
|July 15, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Use of the Wnt/β-catenin Activator Lithium Is Associated with Less Emphysema.

Annals of the American Thoracic Society·2026
Same author

X-inactive specific transcript (XIST) can determine sex differences in cardiovascular drug responses: focus on RNA therapeutics.

Frontiers in pharmacology·2026
Same author

Interferons Inhibit Ebola Virus Infection of Human Keratinocytes.

Viruses·2025
Same author

Dysregulated alveolar type 2 epithelial cell proteostasis promotes fibrogenic macrophage migration inhibitory factor-CD74 signaling.

Science translational medicine·2025
Same author

Immunization with virus-like vesicle-based COVID-19 vaccine induces robust systemic and mucosal immunity.

NPJ vaccines·2025
Same author

EROdicating arterial thrombosis with a novel endoplasmic reticulum oxidoreductase 1α inhibitor.

Molecular therapy : the journal of the American Society of Gene Therapy·2025

Cigarette smoke extract (CSE) inhibits lung fibroblast proliferation. Multiple CSE exposures induce a senescent phenotype, impairing lung repair and potentially contributing to emphysema development in chronic obstructive pulmonary disease (COPD).

Area of Science:

  • Cell Biology
  • Pulmonary Medicine
  • Toxicology

Background:

  • Chronic obstructive pulmonary disease (COPD) is a leading cause of death, with smoking as the primary risk factor.
  • Lung fibroblasts are crucial for tissue repair and homeostasis.
  • Reduced lung fibroblast growth rates are observed in COPD patients.

Purpose of the Study:

  • To investigate the impact of cigarette smoke extract (CSE) on lung fibroblast proliferation.
  • To elucidate the cellular mechanisms underlying CSE-induced changes in fibroblasts.

Main Methods:

  • Exposure of lung fibroblasts to cigarette smoke extract (CSE).
  • Analysis of cell proliferation, cell cycle phases, and key protein pathways (e.g., p53, p16, ATM, p21).
  • Assessment of senescence markers, including morphology and beta-galactosidase activity.

Related Experiment Videos

Main Results:

  • A single CSE exposure inhibited fibroblast proliferation without causing cell death, increasing ATM, p53, and p21 activity.
  • Multiple CSE exposures resulted in profound growth arrest, enlarged cell morphology, and upregulated p16 and senescence-associated beta-galactosidase.
  • These changes indicate a transition to a classic senescent phenotype.

Conclusions:

  • Single CSE exposure inhibits fibroblast proliferation, crucial for lung repair.
  • Multiple CSE exposures induce irreversible fibroblast senescence.
  • Impaired lung repair due to fibroblast senescence may be a key factor in emphysema pathogenesis.