ArticleAtherosclerosis2011
Effects of estrogen on stress-induced premature senescence of vascular smooth muscle cells: a novel mechanism for the "time window theory" of menopausal hormone therapy.
Article in Atherosclerosis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Sex, senescence, senolytics, and cognition.Frontiers in aging neuroscience · 2025Review
- Comprehensive analysis of gene signatures associated with aging in human aortic dissection.Heliyon · 2024Article
- Estrogen Replacement Therapy Induces Antioxidant and Longevity-Related Genes in Women after Medically Induced Menopause.Oxidative medicine and cellular longevity · 2021Article
- Survival of aging CD264Biotechnology and bioengineering · 2020Article
- Decoy TRAIL receptor CD264: a cell surface marker of cellular aging for human bone marrow-derived mesenchymal stem cells.Stem cell research & therapy · 2017Article
- Pathophysiology of Aortic Valve Stenosis: Is It Both Fibrocalcific and Sex Specific?Physiology (Bethesda, Md.) · 2017Review
- 17beta-estradiol Attenuates TNF-α-Induced Premature Senescence of Nucleus Pulposus Cells through Regulating the ROS/NF-κB Pathway.International journal of biological sciences · 2017Article
- Early, but not late onset estrogen replacement therapy prevents oxidative stress and metabolic alterations caused by ovariectomy.Antioxidants & redox signaling · 2014Article
- Physiological roles of mitogen-activated-protein-kinase-activated p38-regulated/activated protein kinase.World journal of biological chemistry · 2011Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo investigate the effects of estrogen on stress-induced premature senescence of vascular smooth muscle cells (VSMCs) and the underlying mechanisms.
methodsVSMCs of passage 2-3 cultured from young (2 months) and old (18 months) female SD rats were induced into premature senescence by exposure to 150 μmol/L H(2)O(2) in the presence or absence of different concentrations of 17β-estradiol (E(2)). The expression or activation of senescence-associated beta-galactosidase (SA-β-Gal), DcR2, oncogene Ras, p38, PRAK, p53, p21, p16 and Rb was detected by flow cytometry, pull-down assay or Western blot.
resultsFlow cytometry analysis showed that in the VSMCs from young rats pre-administration of E(2) significantly suppressed the H(2)O(2)-induced premature senescence (reducing both percentage of SA-β-Gal positive cells and cellular expression of DcR2) in a dose-dependent manner; these senescent-inhibiting effects of E(2) could be blocked by an estrogen receptor antagonist ICI 182,780 (10(-5)mol/L). Pull-down assay or Western blot analysis revealed that pre-administration of 10(-8)mol/L E(2) significantly reduced the H(2)O(2)-induced activation of oncogene Ras, as well as activity of p16 and p38 MAPK, and expression of PRAK, p53, p21 and p-Rb. Unexpectedly, in the VSMCs from old rats the senescent-inhibiting effect of E(2) disappeared and switched to a senescent-promoting action at 10(-8)mol/L. This senescent-promoting effect could be enhanced by ICI 182,780 and eliminated by a cytochrome P450s inhibitor ABT.
conclusionEstrogen inhibits stress-induced premature senescence of VSMCs from young female through its receptor-mediated suppression of both Ras-p38-PRAK-p53-p21-Rb and Ras-p16-Rb pathways, but this effect disappeared and even more switched to a senescent-promoting action in the cells from old body probably due to a side effect of estrogen metabolites.
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