Quantitative effect of 4977 bp deletion of mitochondrial DNA on the susceptibility of human cells to UV-induced apoptosis
Abstract
In this study, we used a series of human cytoplasmic hybrids (cybrids) harboring different proportions of 4977 bp-deleted mtDNA to investigate the quantitative effect of a pathogenic mutation of mtDNA on apoptosis. We found that the sensitivity of human cells to apoptosis triggered by UV irradiation increases with the proportion of 4977 bp-deleted mtDNA. Moreover, UV-induced activation of caspase 3 was preceded by the activation of caspases 8 and 9. Most importantly, we observed that UV-induced cytochrome c release from mitochondria occurred much earlier and was much more pronounced in the cybrids harboring higher proportions of 4977 bp-deleted mtDNA. We suggest that 4977 bp-deleted mtDNA increases the susceptibility of human cells to UV-induced apoptosis in a quantitative manner through cytochrome c release from mitochondria and caspase 3 activation.
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A high proportion of mtDNA deletion rendered human cells more susceptible to UV-induced apoptosis through enhanced release of cytochrome c.
“In one of our previous studies, we showed that a high proportion of mtDNA deletion rendered human cells more susceptible to UV-induced apoptosis through enhanced release of cytochrome c [53].”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [53]
Human skin fibroblasts harboring pathogenic mutations of mtDNA were more susceptible to apoptosis triggered by UV irradiation or oxidative stress.
“We demonstrated that human skin fibroblasts harboring pathogenic mutations of mtDNA were more susceptible to apoptosis triggered by UV irradiation or oxidative stress.”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [53]
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Self-citation
- Authors
- Liu, C.-Y., Lee, C.-F., & Wei, Y.-H.
- Affiliations
- National Yang Ming University (TW)
- Corresponding author
- Wei, Yau-Huei
- ORCID
- Wei, Yau-Huei
- Venue
- Mitochondrion
- Publisher
- Elsevier BV
- Published
- 2007-02
- Volume
- 7
- Issue
- 1-2
- Pages
- 89-95
- ISSN
- 1567-7249 (ISSN-L)
- OpenAlex
- W2086457614
- Cited by
- 33
- References
- 0
- Citations by year
- 2024: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2016: 4 · 2015: 1 · 2014: 2 · 2013: 3 · 2012: 3
- FWCI
- 0.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mitochondrion (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial DNA deletions, UV-induced apoptosis, cytoplasmic hybrids, cytochrome c release, caspase-3 activation, caspase-8, caspase-9, mitochondrial apoptosis, UV sensitivity
- MeSH terms
- DNA, Mitochondrial, Enzyme Activation, Humans, Hybrid Cells, Mitochondria, Oligopeptides, Ultraviolet Rays, Apoptosis, Ophthalmoplegia, Chronic Progressive External, Gene Deletion, Cytochromes c, Caspase 3, Caspase Inhibitors
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