The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts
Open accessAbstract
Sir2, a NAD-dependent deacetylase, modulates lifespan in yeasts, worms and flies. The SIRT1, mammalian homologue of Sir2, regulates signaling for favoring survival in stress. But whether SIRT1 has the function to influence cell viability and senescence under non-stressed conditions in human diploid fibroblasts is far from unknown. Our data showed that enforced SIRT1 expression promoted cell proliferation and antagonized cellular senescence with the characteristic features of delayed Senescence-Associated beta-galactosidase (SA-beta-gal) staining, reduced Senescence-Associated Heterochromatic Foci (SAHF) formation and G1 phase arrest, increased cell growth rate and extended cellular lifespan in human fibroblasts, while dominant-negative SIRT1 allele (H363Y) did not significantly affect cell growth and senescence but displayed a bit decreased lifespan. Western blot results showed that SIRT1 reduced the expression of p16(INK4A) and promoted phosphorylation of Rb. Our data also exposed that overexpression of SIRT1 was accompanied by enhanced activation of ERK and S6K1 signaling. These effects were mimicked in both WI38 cells and 2BS cells by concentration-dependent resveratrol, a SIRT1 activator. It was noted that treatment of SIRT1-.transfected cells with Rapamycin, a mTOR inhibitor, reduced the phosphorylation of S6K1 and the expression of Id1, implying that SIRT1-induced phosphorylation of S6K1 may be partly for the decreased expression of p16(INK4A) and promoted phosphorylation of Rb in 2BS. It was also observed that the expression of SIRT1 and phosphorylation of ERK and S6K1 was declined in senescent 2BS. These findings suggested that SIRT1-promoted cell proliferation and antagonized cellular senescence in human diploid fibroblasts may be, in part, via the activation of ERK/ S6K1 signaling.
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Citations
Cites
Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase
Brunet, A., Sweeney, L. B., Sturgill, J. F., Chua, K. F., Greer, P. L., Lin, Y., Tran, H., Ross, S. E., Mostoslavsky, R., Cohen, H. Y., et al. (2004) · Science · doi:10.1126/science.1094637 · Cited by 3,239
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors
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Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
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“cellular senescence [34].”
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“eukaryotes, including yeasts [3,4], worms [5] and flies [6].”
BackgroundSirtuin activators mimic caloric restriction and delay ageing in metazoans
Wood, J. G., Rogina, B., Lavu, S., Howitz, K., Helfand, S. L., Tatar, M., & Sinclair, D. (2004) · Nature · doi:10.1038/nature02789 · Cited by 1,868
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Ink4a/Arf expression is a biomarker of aging
Krishnamurthy, J., Torrice, C., Ramsey, M. R., Kovalev, G. I., Al-Regaiey, K., Su, L., & Sharpless, N. E. (2004) · Journal of Clinical Investigation · doi:10.1172/jci22475 · Cited by 1,486
Mammalian sirtuins—emerging roles in physiology, aging, and calorie restriction
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Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a
Janzen, V., Forkert, R., Fleming, H. E., Saito, Y., Waring, M. T., Dombkowski, D. M., Cheng, T., DePinho, R. A., Sharpless, N. E., & Scadden, D. T. (2006) · Nature · doi:10.1038/nature05159 · Cited by 1,106
Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing
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“Recent studies discovered that the accumulation of p16 may also, in part, contributed to the physiological aging in vivo, for instance the deterioration of age-associated Haematopoietic stem cells (HSC) functions [19], the declines of olfactory bulb neurogenesis [20] and the restraints of islet regenerative potential…”
Background
Cited by
Mammalian Sirtuins: Biological Insights and Disease Relevance
Haigis, M. C., & Sinclair, D. A. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev.pathol.4.110807.092250 · Cited by 2,085
Trang, P., Wiggins, J. F., Daige, C. L., Cho, C., Omotola, M., Brown, D., Weidhaas, J. B., Bader, A. G., & Slack, F. J. (2011) · Molecular Therapy · doi:10.1038/mt.2011.48 · Cited by 667
SIRT1 Is Essential for Normal Cognitive Function and Synaptic Plasticity
Michan, S., Li, Y., Chou, M. M.-H., Parrella, E., Ge, H., Long, J. M., Allard, J. S., Lewis, K., Miller, M., Xu, W., et al. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.0027-10.2010 · Cited by 541
Sirtuins, a promising target in slowing down the ageing process
Grabowska, W., Sikora, E., & Bielak-Zmijewska, A. (2017) · Biogerontology · doi:10.1007/s10522-017-9685-9 · Cited by 470
Insulin‐like growth factor‐1 regulates the SIRT 1‐p53 pathway in cellular senescence
Tran, D., Bergholz, J., Zhang, H., He, H., Wang, Y., Zhang, Y., Li, Q., Kirkland, J. L., & Xiao, Z. (2014) · Aging Cell · doi:10.1111/acel.12219 · Cited by 161
“Conversely, SIRT1 overexpression antagonizes oncogene-induced cellular senescence in human diploid fibroblasts (Huang et al., 2008), and inhibition of SIRT1 by sirtinol has been shown to induce senescencelike cell growth arrest in human breast cancer MCF7 and human lung adenocarcinoma H1299 cells (Ota et al.”
BackgroundSelf-citation
Metadata
- Authors
- Huang, J., Gan, Q., Han, L., Li, J., Zhang, H., Sun, Y., Zhang, Z., & Tong, T.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2008-03-05
- Volume
- 3
- Issue
- 3
- Pages
- e1710
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W2065667074
- Cited by
- 187
- References
- 14
- FWCI
- 5.94
- Type
- journal article
- Language
- en
- Open access
- gold
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- Huang, J., Gan, Q., Han, L., Li, J., Zhang, H., Sun, Y., Zhang, Z., & Tong, T. (2008). SIRT1 Overexpression Antagonizes Cellular Senescence with Activated ERK/S6k1 Signaling in Human Diploid Fibroblasts. PLoS ONE. https://doi.org/10.1371/journal.pone.0001710
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