Transcriptional and phenotypic changes in aorta and aortic valve with aging and MnSOD deficiency in mice
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The purpose of this study was to characterize changes in antioxidant and age-related gene expression in aorta and aortic valve with aging, and test the hypothesis that increased mitochondrial oxidative stress accelerates age-related endothelial and aortic valve dysfunction. Wild-type (MnSOD(+/+)) and manganese SOD heterozygous haploinsufficient (MnSOD(+/-)) mice were studied at 3 and 18 mo of age. In aorta from wild-type mice, antioxidant expression was preserved, although there were age-associated increases in Nox2 expression. Haploinsufficiency of MnSOD did not alter antioxidant expression in aorta, but increased expression of Nox2. When compared with that of aorta, age-associated reductions in antioxidant expression were larger in aortic valves from wild-type and MnSOD haploinsufficient mice, although Nox2 expression was unchanged. Similarly, sirtuin expression was relatively well-preserved in aorta from both genotypes, whereas expression of SIRT1, SIRT2, SIRT3, SIRT4, and SIRT6 were significantly reduced in the aortic valve. Expression of p16(ink4a), a marker of cellular senescence, was profoundly increased in both aorta and aortic valve from MnSOD(+/+) and MnSOD(+/-) mice. Functionally, we observed comparable age-associated reductions in endothelial function in aorta from both MnSOD(+/+) and MnSOD(+/-) mice. Interestingly, inhibition of NAD(P)H oxidase with apocynin or gp91ds-tat improved endothelial function in MnSOD(+/+) mice but significantly impaired endothelial function in MnSOD(+/-) mice at both ages. Aortic valve function was not impaired by aging or MnSOD haploinsufficiency. Changes in antioxidant and sirtuin gene expression with aging differ dramatically between aorta and aortic valve. Furthermore, although MnSOD does not result in overt cardiovascular dysfunction with aging, compensatory transcriptional responses to MnSOD deficiency appear to be tissue specific.
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Substantial impairment in vascular reactivity is observed in aged mice.
“While only mild cardiac dysfunction has been reported in old mice (Dai et al., 2009; Roos et al., 2013), substantial impairment in vascular reactivity is observed in aged mice (Roos et al., 2013).”
From The Achilles' heel of senescent cells: from transcriptome to senolytic drugs (2015) · cites this paper as Roos et al., 2013
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- Authors
- Roos, C. M., Hagler, M., Zhang, B., Oehler, E. A., Arghami, A., & Miller, J. D.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Miller, Jordan D.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2013-11-15
- Volume
- 305
- Issue
- 10
- Pages
- H1428-H1439
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- PMC
- PMC3840262
- OpenAlex
- W1966990212
- Cited by
- 54
- References
- 42
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 7 · 2020: 2 · 2019: 4 · 2018: 7 · 2017: 5 · 2016: 10 · 2015: 8 · 2014: 2
- FWCI
- 4.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL092235, HL-111121, R01HL111121)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- manganese superoxide dismutase, aging, aorta, aortic valve, mitochondrial oxidative stress, antioxidant gene expression, NADPH oxidase, NOX2, sirtuins, cellular senescence, p16INK4a, endothelial function, apocynin, gp91phox
- MeSH terms
- Superoxide Dismutase 2, Age Factors, Aging, Animals, Antioxidants, Aorta, Thoracic, Aortic Valve, Calcium, Dose-Response Relationship, Drug, Enzyme Inhibitors, Gene Expression Regulation, Genotype, Heterozygote, Mice, Inbred C57BL, Mitochondria, Osteogenesis, Phenotype, Superoxide Dismutase, Transcription, Genetic, Vasodilation, Vasodilator Agents, Cellular Senescence, Mice, Knockout, Oxidative Stress, Inflammation Mediators, Nitric Oxide Synthase, NADPH Oxidases, Cyclin-Dependent Kinase Inhibitor p16, Sirtuins, Mice, Forkhead Transcription Factors, Mice, 129 Strain, Haploinsufficiency
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