SIRT1 contributes to telomere maintenance and augments global homologous recombination

Palacios, José; Herranz, Daniel; Bonis, Maria Luigia De; Llamas‐Velasco, Sara; Serrano, Manuel; Blasco, Marı́a A.

doi:10.1083/jcb.201005160

Cited by 231 publications

(224 citation statements)

References 114 publications

(169 reference statements)

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“…33,42 Further support for this hypothesis is the observation that the deacetylase Sirt1 is selectively expressed in the inner medulla and papilla, and it also is a positive regulator of telomere length, like telomerase. 43 Our observation that osmotic shock, which activates the collecting duct DNA damage response, increased mTert mRNA and protein provides strong support for this possibility.…”

Section: Basic Research Wwwjasnorgmentioning

confidence: 60%

Characterization and Fate of Telomerase-expressing Epithelia during Kidney Repair

Song

Czerniak

Wang

et al. 2011

Journal of the American Society of Nephrology

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After acute kidney injury, mice with short telomeres develop increased damage with reduced proliferative capacity, which suggests an important role for telomere length in kidney repair. The enzyme telomerase reverse transcriptase (mTert) regulates telomere length; embryonic stem cells and certain adult stem cells express mTert, but whether cells in the adult kidney express mTert and whether these cells play a role in renal repair are unknown. Here, we found that telomerase protein and mRNA were highly enriched in renal papilla, a proposed niche of kidney stem cells. Using mTert-GFP reporter mice, we detected mTert in a subset of papillary epithelial cells comprising the collecting duct predominantly but also the loop of Henle. Approximately 5% of mTert-GFP ϩ cells were label retaining, a characteristic of stem cells. mTert mRNA levels increased in renal papilla after ischemia-reperfusion injury, but genetically labeled mTert-expressing papillary cells neither divided nor migrated out of the renal papilla during kidney repair. In summary, these data suggest that cells expressing telomerase reverse transcriptase are not a progenitor-cell population, and they do not play a direct role in kidney repair.

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Section: Basic Research Wwwjasnorgmentioning

confidence: 60%

Characterization and Fate of Telomerase-expressing Epithelia during Kidney Repair

Song

Czerniak

Wang

et al. 2011

Journal of the American Society of Nephrology

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“…5,6 Several studies have demonstrated that SIRT1 prevents the onset of senescence in multiple cell types by interfering with senescence-promoting stress signaling. For instance, SIRT1 inhibits telomere erosion (by interacting with telomere repeats), 86 reduces the production of ROS (by regulating MnSOD through FOXO3), and promotes DNA repair (by activating NBS1 and WRN helicase). 86 -88 In ECs, forced expression of SIRT1 prevents oxidative stress-induced premature senescence, whereas SIRT1 inhibition provokes senescence-like phenotypes.…”

Section: Endothelial Aging Phenotypes Are Regulated By Sirtuins and Fmentioning

confidence: 99%

FOXOs and Sirtuins in Vascular Growth, Maintenance, and Aging

Oellerich

Potente

2012

Circulation Research

136

128

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“…SIRT1 also deacetylates FOXO1, FOXO3a and FOXO4, modulating cell cycle and reactive oxygen species (ROS) generation by increasing p27kip1, MnSOD (manganese superoxide dismutase), and GADD45 (growth arrest and DNA damage inducible protein 45) (Brunet et al, 2004;Daitoku et al, 2004;Kobayashi et al, 2005;van der Horst et al, 2004). Studies in SIRT1-deficient and overexpressing mice identified SIRT1 as a positive regulator of telomere length, and showed that SIRT1 attenuates telomere shortening associated with aging (Palacios et al, 2010).…”

Section: Sirt1mentioning

confidence: 99%

Do Sirtuins Promote Mammalian Longevity?: A Critical Review on Its Relevance to the Longevity Effect Induced by Calorie Restriction

Park

Mori

Shimokawa

2013

Molecules and Cells

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Sirtuins (SIRTs), a family of nicotinamide adenine dinucleotide (NAD)-dependent deacetylases, are emerging as key molecules that regulate aging and age-related diseases including cancers, metabolic disorders, and neurodegenerative diseases. Seven isoforms of SIRT (SIRT1-7) have been identified in mammals. SIRT1 and 6, mainly localized in the nucleus, regulate transcription of genes and DNA repair. SIRT3 in the mitochondria regulates mitochondrial bioenergetics. Initial studies in yeasts, nematodes, and flies indicated a strong connection of SIRT with the life-prolonging effects of calorie restriction (CR), a robust experimental intervention for longevity in a range of organisms. However, subsequent studies reported controversial findings regarding SIRT roles in the effect of CR. This review describes the functional roles of mammalian SIRTs and discusses their relevance to mechanisms underlying the longevity effect of CR.

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SIRT1 contributes to telomere maintenance and augments global homologous recombination

Abstract: SIRT1 is a positive regulator of telomere length and attenuates age-associated telomere shortening.

Cited by 231 publications

References 114 publications

Characterization and Fate of Telomerase-expressing Epithelia during Kidney Repair

Characterization and Fate of Telomerase-expressing Epithelia during Kidney Repair

FOXOs and Sirtuins in Vascular Growth, Maintenance, and Aging

Do Sirtuins Promote Mammalian Longevity?: A Critical Review on Its Relevance to the Longevity Effect Induced by Calorie Restriction

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