Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: Mitochondrial dysfunction is associated with Miro1 reduction in lung epithelial cells by cigarette smoke.

Authors: Sundar, Isaac K; Maremanda, Krishna P; Rahman, Irfan

Published In Toxicol Lett, (2019 Dec 15)

Abstract: Cigarette smoke (CS) is known to cause mitochondrial dysfunction leading to cellular senescence in lung cells. We determined the mechanism of mitochondrial dysfunction by CS in lung epithelial cells. CS extract (CSE) treatment differentially affected mitochondrial function, such as membrane potential, mitochondrial reactive oxygen species (mtROS) and mitochrondrial mass as analyzed by FACS, and were associated with altered oxidative phosphorylation (OXPHOS) protein levels (Complexes I-IV) in primary lung epithelial cells (SAEC and NHBE), and (complexes I and II) in BEAS2B cells. There were dose- and time-dependent changes in mitochondrial respiration (oxygen consumption rate parameters i.e. maximal respiration, ATP production and spare capacity, measured by the Seahorse analyzer) in control vs. CSE treated BEAS2B and NHBE/DHBE cells. Electron microscopy (EM) analysis revealed perinuclear clustering by localization and increased mitochondrial fragmentation by fragement length analysis. Immunoblot analysis revealed CS-mediated increase in Drp1 and decrease in Mfn2 levels that are involved in mitochondrial fission/fusion process. CSE treatment reduced Miro1 and Pink1 abundance that play a crucial role in the intercellular transfer mechanism and mitophagy process. Overall, these findings highlight the role of Miro1 in context of CS-induced mitochondrial dysfunction in lung epithelial cells that may contribute to the pathogenesis of chronic inflammatory lung diseases.

PubMed ID: 31593750 Exiting the NIEHS site

MeSH Terms: Case-Control Studies; Cells, Cultured; Cigarette Smoking/adverse effects*; Down-Regulation; Energy Metabolism; Epithelial Cells/metabolism*; Epithelial Cells/ultrastructure; Humans; Lung/metabolism*; Lung/ultrastructure; Mitochondria/metabolism*; Mitochondria/ultrastructure; Mitochondrial Proteins/metabolism*; Mitophagy; Oxidative Stress; Pulmonary Disease, Chronic Obstructive/etiology*; Pulmonary Disease, Chronic Obstructive/metabolism; Pulmonary Disease, Chronic Obstructive/pathology; Signal Transduction; Smoke/adverse effects*; rho GTP-Binding Proteins/metabolism*

Back
to Top