The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
PARK2-mediated mitophagy is involved in regulation of HBEC senescence in COPD pathogenesis
Open accessAbstract
Cigarette smoke (CS)-induced mitochondrial damage with increased reactive oxygen species (ROS) production has been implicated in COPD pathogenesis by accelerating senescence. Mitophagy may play a pivotal role for removal of CS-induced damaged mitochondria, and the PINK1 (PTEN-induced putative kinase 1)-PARK2 pathway has been proposed as a crucial mechanism for mitophagic degradation. Therefore, we sought to investigate to determine if PINK1-PARK2-mediated mitophagy is involved in the regulation of CS extract (CSE)-induced cell senescence and in COPD pathogenesis. Mitochondrial damage, ROS production, and cell senescence were evaluated in primary human bronchial epithelial cells (HBEC). Mitophagy was assessed in BEAS-2B cells stably expressing EGFP-LC3B, using confocal microscopy to measure colocalization between TOMM20-stained mitochondria and EGFP-LC3B dots as a representation of autophagosome formation. To elucidate the involvement of PINK1 and PARK2 in mitophagy, knockdown and overexpression experiments were performed. PINK1 and PARK2 protein levels in lungs from patients were evaluated by means of lung homogenate and immunohistochemistry. We demonstrated that CSE-induced mitochondrial damage was accompanied by increased ROS production and HBEC senescence. CSE-induced mitophagy was inhibited by PINK1 and PARK2 knockdown, resulting in enhanced mitochondrial ROS production and cellular senescence in HBEC. Evaluation of protein levels demonstrated decreased PARK2 in COPD lungs compared with non-COPD lungs. These results suggest that PINK1-PARK2 pathway-mediated mitophagy plays a key regulatory role in CSE-induced mitochondrial ROS production and cellular senescence in HBEC. Reduced PARK2 expression levels in COPD lung suggest that insufficient mitophagy is a part of the pathogenic sequence of COPD.
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LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing.
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PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
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Yoshida, M., Minagawa, S., Araya, J., Sakamoto, T., Hara, H., Tsubouchi, K., Hosaka, Y., Ichikawa, A., Saito, N., Kadota, T., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10991-7 · Cited by 572
Self-citationAutophagy and inflammation in chronic respiratory disease
Racanelli, A. C., Kikkers, S. A., Choi, A. M. K., & Cloonan, S. M. (2018) · Autophagy · doi:10.1080/15548627.2017.1389823 · Cited by 547
Yao, R.-Q., Ren, C., Xia, Z.-F., & Yao, Y.-M. (2021) · Autophagy · doi:10.1080/15548627.2020.1725377 · Cited by 441
Cloonan, S. M., & Choi, A. M. K. (2016) · Journal of Clinical Investigation · doi:10.1172/jci81113 · Cited by 322
Cellular Metabolism in Lung Health and Disease
Liu, G., & Summer, R. (2019) · Annual Review of Physiology · doi:10.1146/annurev-physiol-020518-114640 · Cited by 157
Metadata
- Authors
- Ito, S., Araya, J., Kurita, Y., Kobayashi, K., Takasaka, N., Yoshida, M., Hara, H., Minagawa, S., Wakui, H., Fujii, S., Kojima, J., Shimizu, K., Numata, T., Kawaishi, M., Odaka, M., Morikawa, T., Harada, T., Nishimura, S. L., Kaneko, Y., Nakayama, K., & Kuwano, K.
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2015-02-25
- Volume
- 11
- Issue
- 3
- Pages
- 547-559
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- OpenAlex
- W1586820518
- Cited by
- 274
- References
- 47
- FWCI
- 15.60
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Ito, S., Araya, J., Kurita, Y., Kobayashi, K., Takasaka, N., Yoshida, M., Hara, H., Minagawa, S., Wakui, H., Fujii, S., Kojima, J., Shimizu, K., Numata, T., Kawaishi, M., Odaka, M., Morikawa, T., Harada, T., Nishimura, S. L., Kaneko, Y., . . . Kuwano, K. (2015). PARK2-mediated mitophagy is involved in regulation of HBEC senescence in COPD pathogenesis. Autophagy. https://doi.org/10.1080/15548627.2015.1017190
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