MiR-23a-depressed autophagy is a participant in PUVA- and UVB-induced premature senescence
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// Jia-an Zhang 1,* , Bing-rong Zhou 1,2,* , Yang Xu 1 , Xu Chen 2,3 , Juan Liu 1 , Maya Gozali 1 , Di Wu 1 , Zhi-qiang Yin 1 and Dan Luo 1 1 Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China 2 Jiangsu Provincial Key Laboratory of Molecular Biology for Skin Diseases and STIs, Nanjing, Jiangsu, China 3 Institute of Dermatology, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College (PUMC), Nanjing, Jiangsu, China * These authors have contributed equally to this work Correspondence to: Bing-rong Zhou, email: // Dan Luo, email: // Keywords : autophagy, stress-induced premature senescence, miR-23a, AMBRA1, ultraviolet, Gerotarget Received : September 17, 2015 Accepted : May 05, 2016 Published : May 13, 2016 Abstract Autophagy is a cellular catabolic mechanism that is activated in response to stress conditions, including ultraviolet (UV) irradiation, starvation, and misfolded protein accumulation. Abnormalities in autophagy are associated with several pathologies, including aging and cancer. Furthermore, recent studies have demonstrated that microRNAs (miRNAs) are potent modulators of the autophagy pathway. As a result, the current study aims to elucidate the role of the autophagy-related miRNA miR-23ain the process of photoaging. Experiments demonstrated that the antagomir-mediated inactivation of miR-23a resulted in the stimulation of PUVA- and UVB-depressed autophagy flux and protected human fibroblasts from premature senescence. Furthermore, AMBRA1 was identified as a miR-23a target. AMBRA1 cellular levels increased following the introduction of miR-23a antagomirs. And a bioinformatics analysis revealed that the AMBRA1 3’ UTR contains functional miR-23a responsive sequences. Finally, it was also demonstrated that both AMBRA1 overexpression and Rapamycin treatment were both able to rescue fibroblasts from PUVA and UVB irradiation-induced autophagy inhibition, but that these effects could also be mitigated by miR-23a overexpression. Therefore, this study concludes that miR-23a-regulated autophagy is a novel and important regulator of ultraviolet-induced premature senescence and AMBRA1 is a rate-limiting miRNA target in this pathway.
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miR-23a, miR-23b, and miR-24 suppress AMBRA1, ATG12, and ATG4A, respectively.
“For example, miR-23a, miR-23b, and miR-24 suppress AMBRA1 [52], ATG12 [53, 54], and ATG4A [55], respectively.”
From miR-27a and miR-27b regulate autophagic clearance of damaged mitochondria by targeting PTEN-induced putative kinase 1 (PINK1) (2016) · cites this paper as [52]
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- Authors
- Zhang, J.-A., Zhou, B.-R., Xu, Y., Chen, X., Liu, J., Gozali, M., Wu, D., Yin, Z.-Q., & Luo, D.
- Affiliations
- Jiangsu Province Hospital (CN)
- Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Corresponding author
- Zhang, Jia-an
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2016-05-13
- Volume
- 7
- Issue
- 25
- Pages
- 37420-37435
- ISSN
- 1949-2553 (ISSN-L)
- PMC
- PMC5122322
- OpenAlex
- W2386447396
- Cited by
- 53
- References
- 36
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 3 · 2022: 4 · 2021: 8 · 2020: 8 · 2019: 9 · 2018: 3 · 2017: 8 · 2016: 2
- FWCI
- 6.88
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Oncotarget (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Government of Jiangsu Province
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- miR-23a, autophagy, stress-induced premature senescence, photoaging, PUVA, UV-B radiation, AMBRA1, microRNA, rapamycin, human fibroblasts, 3' untranslated region, antagomir, skin aging, skin aging biomarkers, aging biomarkers
- MeSH terms
- Antagomirs, Autophagy, Fibroblasts, Humans, Skin, Skin Physiological Phenomena, Transfection, Skin Aging, Cellular Senescence, MicroRNAs, Adaptor Proteins, Signal Transducing
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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