Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.

American Journal of Respiratory Cell and Molecular Biology
Zhengke WangQing Lu

Abstract

Cigarette smoke (CS) exposure increases the risk for acute respiratory distress syndrome in humans and promotes alveolar-capillary barrier permeability and acute lung injury in animal models. However, the underlying mechanisms are not well understood. Mitochondrial fusion and fission are essential for mitochondrial homeostasis in health and disease. In this study, we hypothesized that CS caused endothelial injury via an imbalance of mitochondrial fusion and fission and resultant mitochondrial oxidative stress and dysfunction. We noted that CS altered mitochondrial morphology by shortening mitochondrial networks and causing perinuclear accumulation of damaged mitochondria in primary rat lung microvascular endothelial cells. We also found that CS increased mitochondrial fission likely by decreasing Drp1-S637 and increasing FIS1, Drp1-S616 phosphorylation, mitochondrial translocation, and tetramerization and reduced mitochondrial fusion likely by decreasing Mfn2 in lung microvascular endothelial cells and mouse lungs. CS also caused aberrant mitophagy, increased mitochondrial oxidative stress, and reduced mitochondrial respiration. An inhibitor of mitochondrial fission and a mitochondria-specific antioxidant prevented CS-induced i...Continue Reading

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Citations

Dec 3, 2020·Frontiers in Cell and Developmental Biology·Jia Zheng, Chengzhi Lu
Oct 27, 2020·American Journal of Respiratory Cell and Molecular Biology·Kazuya Tanimura, Toru Nyunoya

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Methods Mentioned

BETA
GTPases
Fluorescence
flow cytometry
X-ray
fluorescence microscopy
GTPase
fluorescence spectrometry

Software Mentioned

image J
Graphpad Prism

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