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Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence.
Am J Physiol Lung Cell Mol Physiol. 2013 Nov 15; 305(10):L737-46.AJ

Abstract

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.

Authors+Show Affiliations

Division of Respiratory diseases, Dept. of Internal Medicine, Jikei Univ. School of Medicine, Japan. hirohara@jikei.ac.jp.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24056969

Citation

Hara, Hiromichi, et al. "Mitochondrial Fragmentation in Cigarette Smoke-induced Bronchial Epithelial Cell Senescence." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 305, no. 10, 2013, pp. L737-46.
Hara H, Araya J, Ito S, et al. Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. Am J Physiol Lung Cell Mol Physiol. 2013;305(10):L737-46.
Hara, H., Araya, J., Ito, S., Kobayashi, K., Takasaka, N., Yoshii, Y., Wakui, H., Kojima, J., Shimizu, K., Numata, T., Kawaishi, M., Kamiya, N., Odaka, M., Morikawa, T., Kaneko, Y., Nakayama, K., & Kuwano, K. (2013). Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. American Journal of Physiology. Lung Cellular and Molecular Physiology, 305(10), L737-46. https://doi.org/10.1152/ajplung.00146.2013
Hara H, et al. Mitochondrial Fragmentation in Cigarette Smoke-induced Bronchial Epithelial Cell Senescence. Am J Physiol Lung Cell Mol Physiol. 2013 Nov 15;305(10):L737-46. PubMed PMID: 24056969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. AU - Hara,Hiromichi, AU - Araya,Jun, AU - Ito,Saburo, AU - Kobayashi,Kenji, AU - Takasaka,Naoki, AU - Yoshii,Yutaka, AU - Wakui,Hiroshi, AU - Kojima,Jun, AU - Shimizu,Kenichiro, AU - Numata,Takanori, AU - Kawaishi,Makoto, AU - Kamiya,Noriki, AU - Odaka,Makoto, AU - Morikawa,Toshiaki, AU - Kaneko,Yumi, AU - Nakayama,Katsutoshi, AU - Kuwano,Kazuyoshi, Y1 - 2013/09/20/ PY - 2013/9/24/entrez PY - 2013/9/24/pubmed PY - 2014/1/23/medline KW - chronic obstructive pulmonary disease KW - mitochondria dynamics SP - L737 EP - 46 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am J Physiol Lung Cell Mol Physiol VL - 305 IS - 10 N2 - 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. SN - 1522-1504 UR - https://www.unboundmedicine.com/medline/citation/24056969/Mitochondrial_fragmentation_in_cigarette_smoke_induced_bronchial_epithelial_cell_senescence_ DB - PRIME DP - Unbound Medicine ER -