miR-34a promotes fibrosis in aged lungs by inducing alveolarepithelial dysfunctions
Open accessAbstract
Idiopathic pulmonary fibrosis is a well-known age-related disease. However, much less recognized has been the aging associated pathogenesis of this disorder. As we and others previously showed that dysregulation of micro-RNAs (miRNAs) was an important mechanism involved in pulmonary fibrosis, the role of these molecules in this pathology in the aged population has not been investigated (Cushing L, Kuang PP, Qian J, Shao F, Wu J, Little F, Thannickal VJ, Cardoso WV, Lü J. Am J Respir Cell Mol Biol 45: 287–294, 2011; Liu G, Friggeri A, Yang Y, Milosevic J, Ding Q, Thannickal VJ, Kaminski N, Abraham E. J Exp Med 207: 1589–1597, 2010; Pandit KV, Corcoran D, Yousef H, Yarlagadda M, Tzouvelekis A, Gibson KF, Konishi K, Yousem SA, Singh M, Handley D, Richards T, Selman M, Watkins SC, Pardo A, Ben-Yehudah A, Bouros D, Eickelberg O, Ray P, Benos PV, Kaminski N. Am J Respir Crit Care Med 182: 220–229, 2010). In this study, by using a lung fibrosis model established in old mice, we found that ablation of miR-34a protected aged animals from developing experimental lung fibrosis. miR-34a was upregulated in lung epithelial cells, but not in lung fibroblasts of aged mice, and miR-34a expression was further increased in epithelial cells of the fibrotic lungs of these old animals. We found that miR-34a induced dysfunctions in alveolar epithelial cells (AECs), as evidenced by increased cellular senescence and apoptosis and mitochondrial aberrations. More importantly, these abnormalities were attenuated in AECs of the fibrotic lungs of aged miR-34a−/− mice. We found that miR-34a targeted Sirt1, a master anti-aging regulator, and two key cell cycle modulators, E2F3 and cyclin E2, in lung epithelial cells, and the repression of these targets was relieved in miR-34a-deficient AECs. In summary, our data suggest that elevated AEC miR-34a plays a critical role in the pathogenesis of pulmonary fibrosis in the aged population. Our study also indicates miR-34a to be a more precise miRNA target for treating this disease that overwhelmingly affects people of advanced age.
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Epithelial cell senescence is detrimental, whereas fibroblast senescence is protective.
“indicating that epithelial cell senescence is indeed detrimental, whereas fibroblast senescence is protective.”
From Senolytic drugs target alveolar epithelial cell function and attenuate experimental lung fibrosis <i>ex vivo</i> (2017) · cites this paper as [43]
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- Authors
- Cui, H., Ge, J., Xie, N., Banerjee, S., Zhou, Y., Liu, R.-M., Thannickal, V. J., & Liu, G.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Liu, Gang
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2017-03-01
- Volume
- 312
- Issue
- 3
- Pages
- L415-L424
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- PMC
- PMC5374304
- OpenAlex
- W2564479815
- Cited by
- 66
- References
- 47
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 5 · 2023: 5 · 2022: 9 · 2021: 6 · 2020: 12 · 2019: 8 · 2018: 7 · 2017: 4
- FWCI
- 5.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI) (HL105473, HL126737, HL114470)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Keywords
- idiopathic pulmonary fibrosis, lung aging, alveolar epithelial cells, cellular senescence, apoptosis, mitochondrial dysfunction, SIRT1, E2F3, cyclin E2, age-related diseases, cell cycle regulation
- MeSH terms
- Aging, Animals, Bleomycin, Cell Line, Fibroblasts, Humans, Mitochondria, Phenotype, Up-Regulation, Cellular Senescence, Apoptosis, MicroRNAs, Cell Proliferation, Mice, Idiopathic Pulmonary Fibrosis, Alveolar Epithelial Cells
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