The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Mitochondrial DNA Integrity Is Essential For Mitochondrial Maturation During Differentiation of Neural Stem Cells
Abstract
Differentiation of neural stem cells (NSCs) involves the activation of aerobic metabolism, which is dependent on mitochondrial function. Here, we show that the differentiation of NSCs involves robust increases in mitochondrial mass, mitochondrial DNA (mtDNA) copy number, and respiration capacity. The increased respiration activity renders mtDNA vulnerable to oxidative damage, and NSCs defective for the mitochondrial 8-oxoguanine DNA glycosylase (OGG1) function accumulate mtDNA damage during the differentiation. The accumulated mtDNA damages in ogg1−/− cells inhibit the normal maturation of mitochondria that is manifested by reduced cellular levels of mitochondrial encoded complex proteins (complex I [cI], cIII, and cIV) with normal levels of the nuclear encoded cII present. The specific cI activity and inner membrane organization of respiratory complexes are similar in wt and ogg1−/− cells, inferring that mtDNA damage manifests itself as diminished mitochondrial biogenesis rather than the generation of dysfunctional mitochondria. Aerobic metabolism increases during differentiation in wild-type cells and to a lesser extent in ogg1−/− cells, whereas anaerobic rates of metabolism are constant and similar in both cell types. Our results demonstrate that mtDNA integrity is essential for effective mitochondrial maturation during NSC differentiation.
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Cites
AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity
Cantó, C., Gerhart-Hines, Z., Feige, J. N., Lagouge, M., Noriega, L., Milne, J. C., Elliott, P. J., Puigserver, P., & Auwerx, J. (2009) · Nature · doi:10.1038/nature07813 · Cited by 3,300
Mitochondrial transcription factor A regulates mtDNA copy number in mammals
Ekstrand, M. I. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddh109 · Cited by 919
Yadava, N., & Nicholls, D. G. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.0212-07.2007 · Cited by 272
Accumulation of mitochondrial DNA damage and bioenergetic dysfunction in CSB defective cells
Osenbroch, P. Ø., Auk‐Emblem, P., Halsne, R., Strand, J., Forstrøm, R. J., van der Pluijm, I., & Eide, L. (2009) · The FEBS Journal · doi:10.1111/j.1742-4658.2009.07004.x · Cited by 60
Self-citationLuo, G.-F., Yu, T.-Y., Wen, X.-H., Li, Y., & Yang, G.-S. (2007) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-007-9587-2 · Cited by 28
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Functional consequences of developmentally regulated alternative splicing
Kalsotra, A., & Cooper, T. A. (2011) · Nature Reviews Genetics · doi:10.1038/nrg3052 · Cited by 729
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Role of Oct4 in maintaining and regaining stem cell pluripotency
Shi, G., & Jin, Y. (2010) · Stem Cell Research & Therapy · doi:10.1186/scrt39 · Cited by 294
The role of mitochondria in stem cell fate and aging
Zhang, H., Menzies, K. J., & Auwerx, J. (2018) · Development · doi:10.1242/dev.143420 · Cited by 284
Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting
Huang, Z., Cheng, L., Guryanova, O. A., Wu, Q., & Bao, S. (2010) · Protein & Cell · doi:10.1007/s13238-010-0078-y · Cited by 248
Regulation of glioblastoma stem cells by retinoic acid: role for Notch pathway inhibition
Ying, M., Wang, S., Sang, Y., Sun, P., Lal, B., Goodwin, C. R., Guerrero-Cazares, H., Quinones-Hinojosa, A., Laterra, J., & Xia, S. (2011) · Oncogene · doi:10.1038/onc.2011.58 · Cited by 204
Matkarimov, B. T., & Saparbaev, M. K. (2020) · Advances in Experimental Medicine and Biology · doi:10.1007/978-3-030-41283-8_6 · Cited by 18
Metadata
- Authors
- Wang, W., Osenbroch, P., Skinnes, R., Esbensen, Y., Bjørås, M., & Eide, L.
- Venue
- Stem Cells
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-12-01
- Volume
- 28
- Issue
- 12
- Pages
- 2195-2204
- ISSN
- 1066-5099 (ISSN-L)
- 1549-4918
- OpenAlex
- W2082075729
- Cited by
- 243
- References
- 5
- FWCI
- 9.92
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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