Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence
| العنوان: | Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence |
|---|---|
| المؤلفون: | Naoki Takasaka, Kenichiro Shimizu, Toshiaki Morikawa, Hiroshi Wakui, Kazuyoshi Kuwano, Jun Kojima, Yumi Kaneko, Jun Araya, Yutaka Yoshii, Hiromichi Hara, Katsutoshi Nakayama, Noriki Kamiya, Makoto Odaka, Saburo Ito, Makoto Kawaishi, Takanori Numata, Kenji Kobayashi |
| المصدر: | American journal of physiology. Lung cellular and molecular physiology. 305(10) |
| سنة النشر: | 2013 |
| مصطلحات موضوعية: | Pulmonary and Respiratory Medicine, Senescence, Dynamins, Physiology, Blotting, Western, Bronchi, Mitochondrion, Biology, Mitochondrial fragmentation, GTP Phosphohydrolases, Immunoenzyme Techniques, Mitochondrial Proteins, Physiology (medical), Organelle, Tobacco, Cigarette smoke, Humans, RNA, Small Interfering, Cells, Cultured, Cellular Senescence, Membrane Proteins, Epithelial Cells, Cell Biology, Bronchial Epithelial Cell, Cell biology, Mitochondria, Microscopy, Electron, Reactive Oxygen Species, Microtubule-Associated Proteins |
| الوصف: | Mitochondria are dynamic organelles that continuously change their shape through fission and fusion. Disruption of mitochondrial dynamics is involved in disease pathology through excessive reactive oxygen species (ROS) production. Accelerated cellular senescence resulting from cigarette smoke exposure with excessive ROS production has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Hence, we investigated the involvement of mitochondrial dynamics and ROS production in terms of cigarette smoke extract (CSE)-induced cellular senescence in human bronchial epithelial cells (HBEC). Mitochondrial morphology was examined by electron microscopy and fluorescence microscopy. Senescence-associated β-galactosidase staining and p21 Western blotting of primary HBEC were performed to evaluate cellular senescence. Mitochondrial-specific superoxide production was measured by MitoSOX staining. Mitochondrial fragmentation was induced by knockdown of mitochondrial fusion proteins (OPA1 or Mitofusins) by small-interfering RNA transfection. N-acetylcysteine and Mito-TEMPO were used as antioxidants. Mitochondria in bronchial epithelial cells were prone to be more fragmented in COPD lung tissues. CSE induced mitochondrial fragmentation and mitochondrial ROS production, which were responsible for acceleration of cellular senescence in HBEC. Mitochondrial fragmentation induced by knockdown of fusion proteins also increased mitochondrial ROS production and percentages of senescent cells. HBEC senescence and mitochondria fragmentation in response to CSE treatment were inhibited in the presence of antioxidants. CSE-induced mitochondrial fragmentation is involved in cellular senescence through the mechanism of mitochondrial ROS production. Hence, disruption of mitochondrial dynamics may be a part of the pathogenic sequence of COPD development. |
| تدمد: | 1522-1504 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5bcaa3b934c319c240011d343663f86fTest https://pubmed.ncbi.nlm.nih.gov/24056969Test |
| رقم الانضمام: | edsair.doi.dedup.....5bcaa3b934c319c240011d343663f86f |
| قاعدة البيانات: | OpenAIRE |
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Disruption of mitochondrial dynamics is involved in disease pathology through excessive reactive oxygen species (ROS) production. Accelerated cellular senescence resulting from cigarette smoke exposure with excessive ROS production has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Hence, we investigated the involvement of mitochondrial dynamics and ROS production in terms of cigarette smoke extract (CSE)-induced cellular senescence in human bronchial epithelial cells (HBEC). Mitochondrial morphology was examined by electron microscopy and fluorescence microscopy. Senescence-associated β-galactosidase staining and p21 Western blotting of primary HBEC were performed to evaluate cellular senescence. Mitochondrial-specific superoxide production was measured by MitoSOX staining. Mitochondrial fragmentation was induced by knockdown of mitochondrial fusion proteins (OPA1 or Mitofusins) by small-interfering RNA transfection. 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