Cited by 303Sirtuins and Resveratrol in MedicineTelomeres, Telomerase, and SenescenceNitric Oxide and Endothelin Effects

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SIRT1 Promotes Proliferation and Prevents Senescence Through Targeting LKB1 in Primary Porcine Aortic Endothelial Cells

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Zu, Yi, Liu, Ling, Lee, Mary Y.K., Xu, Cheng, Liang, Yan, Man, Ricky Y., Vanhoutte, Paul M., Wang, Yu·2010·Circulation Research

DOI 10.1161/circresaha.109.215483

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Abstract

RATIONALE: Endothelial senescence causes endothelial dysfunction, promotes atherogenesis and contributes to age-related vascular disorders. SIRT1 is a conserved NAD(+)-dependent deacetylase possessing beneficial effects against aging-related diseases, despite that the detailed functional mechanisms are largely uncharacterized. OBJECTIVE: The present study is designed to evaluate the protective effects of SIRT1 on endothelial senescence and to elucidate the underlying mechanisms. METHODS AND RESULTS: An in vitro senescence model was established by prolonged culture of primary endothelial cells isolated from porcine aorta. The freshly isolated "young" cells gradually underwent senescence during 1 month of repetitive passages. Both mRNA and protein expressions of SIRT1 were progressively decreased. In contrast, the protein levels of LKB1, a serine/threonine kinase and tumor suppressor, and the phosphorylation of its downstream target AMPK(Thr172) were dramatically increased in senescent cells. Overexpression of LKB1 promoted cellular senescence and retarded endothelial proliferation, which could be blocked by increasing SIRT1 levels. Knocking down of SIRT1 induced senescence and elevated the protein levels of LKB1 and phosphorylated AMPK(Thr172). Regardless of the nutritional status, hyperactivation of AMPK was able to induce endothelial senescence. SIRT1 antagonized LKB1-dependent AMPK activation through promoting the deacetylation, ubiquitination and proteasome-mediated degradation of LKB1. The survival signaling of Akt was also found to be modulated by SIRT1 and LKB1, and could cross-regulate AMPK activity. CONCLUSIONS: SIRT1 and LKB1/AMPK are the 2 key sensor systems for regulating endothelial cell survival, proliferation and senescence. The protective activities of SIRT1 may be achieved at least in part by fine tuning the acetylation/deacetylation status and stabilities of LKB1 protein.

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Authors: Zu, Y., Liu, L., Lee, M. Y. K., Xu, C., Liang, Y., Man, R. Y., Vanhoutte, P. M., & Wang, Y.
Affiliations: University of Hong Kong (HK)
ORCID: Liu, Ling
Lee, Mary Y.K.
Xu, Cheng
Liang, Yan
Vanhoutte, Paul M.
Wang, Yu
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2010-04-30
Volume: 106
Issue: 8
Pages: 1384-1393
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/circresaha.109.215483
OpenAlex: W1964041100
Cited by: 303
References: 48
Citations by year: 2026: 9 · 2025: 13 · 2024: 11 · 2023: 13 · 2022: 25 · 2021: 19 · 2020: 21 · 2019: 15 · 2018: 23 · 2017: 16 · 2016: 19 · 2015: 24 · 2014: 25 · 2013: 20 · 2012: 28
FWCI: 8.91
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
Topics: Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords: SIRT1, LKB1, AMPK, endothelial cell senescence, endothelial cell proliferation, endothelial cell survival, protein deacetylation, ubiquitination, proteasomal degradation, Akt signaling, aortic endothelial cells, atherogenesis
MeSH terms: Acetylation, Animals, Aorta, Cell Survival, Cells, Cultured, Enzyme Activation, Female, Genotype, Humans, Injections, Intraperitoneal, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Paraquat, Phenotype, Phosphorylation, Protein Processing, Post-Translational, RNA, Messenger, Swine, Threonine, Time Factors, Transfection, Signal Transduction, Down-Regulation, Up-Regulation, Cellular Senescence, Protein Serine-Threonine Kinases, RNA Interference, Endothelial Cells, Proteasome Endopeptidase Complex, Cell Proliferation, Proto-Oncogene Proteins c-akt, Mice, Ubiquitination, AMP-Activated Protein Kinases, Sirtuin 1

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SIRT1 Promotes Proliferation and Prevents Senescence Through Targeting LKB1 in Primary Porcine Aortic Endothelial Cells

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