Nicotinamide mononucleotide (NMN) treatment attenuates oxidative stress and rescues angiogenic capacity in aged cerebromicrovascular endothelial cells: a potential mechanism for the prevention of vascular cognitive impairment
Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD + depletion in the vasculature and that administratio...
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| Published in | GeroScience Vol. 41; no. 5; pp. 619 - 630 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Springer International Publishing
01.10.2019
Springer Nature B.V |
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| Abstract | Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD
+
depletion in the vasculature and that administration of NAD
+
precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD
+
intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demonstrated that compared with young cells, aged CMVECs exhibit impaired proliferation, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology), impaired ability to form capillary-like structures, and increased oxidative stress. NMN treatment in aged CMVECs significantly improved angiogenic processes and attenuated H
2
O
2
production. We also found that pre-treatment with EX-527, a pharmacological inhibitor of SIRT1, prevented NMN-mediated restoration of angiogenic processes in aged CMVECs. Collectively, we find that normal cellular NAD
+
levels are essential for normal endothelial angiogenic processes, suggesting that age-related cellular NAD
+
depletion and consequential SIRT1 dysregulation may be a potentially reversible mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging. We recommend that pro-angiogenic effects of NAD
+
boosters should be considered in both preclinical and clinical studies. |
|---|---|
| AbstractList | Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD
depletion in the vasculature and that administration of NAD
precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD
intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demonstrated that compared with young cells, aged CMVECs exhibit impaired proliferation, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology), impaired ability to form capillary-like structures, and increased oxidative stress. NMN treatment in aged CMVECs significantly improved angiogenic processes and attenuated H
O
production. We also found that pre-treatment with EX-527, a pharmacological inhibitor of SIRT1, prevented NMN-mediated restoration of angiogenic processes in aged CMVECs. Collectively, we find that normal cellular NAD
levels are essential for normal endothelial angiogenic processes, suggesting that age-related cellular NAD
depletion and consequential SIRT1 dysregulation may be a potentially reversible mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging. We recommend that pro-angiogenic effects of NAD
boosters should be considered in both preclinical and clinical studies. Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD+ depletion in the vasculature and that administration of NAD+ precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demonstrated that compared with young cells, aged CMVECs exhibit impaired proliferation, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology), impaired ability to form capillary-like structures, and increased oxidative stress. NMN treatment in aged CMVECs significantly improved angiogenic processes and attenuated H2O2 production. We also found that pre-treatment with EX-527, a pharmacological inhibitor of SIRT1, prevented NMN-mediated restoration of angiogenic processes in aged CMVECs. Collectively, we find that normal cellular NAD+ levels are essential for normal endothelial angiogenic processes, suggesting that age-related cellular NAD+ depletion and consequential SIRT1 dysregulation may be a potentially reversible mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging. We recommend that pro-angiogenic effects of NAD+ boosters should be considered in both preclinical and clinical studies.Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD+ depletion in the vasculature and that administration of NAD+ precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demonstrated that compared with young cells, aged CMVECs exhibit impaired proliferation, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology), impaired ability to form capillary-like structures, and increased oxidative stress. NMN treatment in aged CMVECs significantly improved angiogenic processes and attenuated H2O2 production. We also found that pre-treatment with EX-527, a pharmacological inhibitor of SIRT1, prevented NMN-mediated restoration of angiogenic processes in aged CMVECs. Collectively, we find that normal cellular NAD+ levels are essential for normal endothelial angiogenic processes, suggesting that age-related cellular NAD+ depletion and consequential SIRT1 dysregulation may be a potentially reversible mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging. We recommend that pro-angiogenic effects of NAD+ boosters should be considered in both preclinical and clinical studies. Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD+ depletion in the vasculature and that administration of NAD+ precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demonstrated that compared with young cells, aged CMVECs exhibit impaired proliferation, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology), impaired ability to form capillary-like structures, and increased oxidative stress. NMN treatment in aged CMVECs significantly improved angiogenic processes and attenuated H2O2 production. We also found that pre-treatment with EX-527, a pharmacological inhibitor of SIRT1, prevented NMN-mediated restoration of angiogenic processes in aged CMVECs. Collectively, we find that normal cellular NAD+ levels are essential for normal endothelial angiogenic processes, suggesting that age-related cellular NAD+ depletion and consequential SIRT1 dysregulation may be a potentially reversible mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging. We recommend that pro-angiogenic effects of NAD+ boosters should be considered in both preclinical and clinical studies. Age-related impairment of angiogenesis likely has a critical role in cerebromicrovascular rarefaction and development of vascular cognitive impairment and dementia (VCID) in the elderly. Recently, we demonstrated that aging is associated with NAD + depletion in the vasculature and that administration of NAD + precursors exerts potent anti-aging vascular effects, rescuing endothelium-mediated vasodilation in the cerebral circulation and improving cerebral blood supply. The present study was designed to elucidate how treatment with nicotinamide mononucleotide (NMN), a key NAD + intermediate, impacts age-related impairment of endothelial angiogenic processes. Using cerebromicrovascular endothelial cells (CMVECs) isolated from young and aged F344xBN rats, we demonstrated that compared with young cells, aged CMVECs exhibit impaired proliferation, cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology), impaired ability to form capillary-like structures, and increased oxidative stress. NMN treatment in aged CMVECs significantly improved angiogenic processes and attenuated H 2 O 2 production. We also found that pre-treatment with EX-527, a pharmacological inhibitor of SIRT1, prevented NMN-mediated restoration of angiogenic processes in aged CMVECs. Collectively, we find that normal cellular NAD + levels are essential for normal endothelial angiogenic processes, suggesting that age-related cellular NAD + depletion and consequential SIRT1 dysregulation may be a potentially reversible mechanism underlying impaired angiogenesis and cerebromicrovascular rarefaction in aging. We recommend that pro-angiogenic effects of NAD + boosters should be considered in both preclinical and clinical studies. |
| Author | Csipo, Tamas Ungvari, Zoltan Zhang, Xin A. Csiszar, Anna Yabluchanskiy, Andriy Valcarcel-Ares, Marta Noa Tarantini, Stefano Balasubramanian, Priya Farkas, Eszter Lipecz, Agnes Reglodi, Dora Bari, Ferenc Kiss, Tamas |
| Author_xml | – sequence: 1 givenname: Tamas surname: Kiss fullname: Kiss, Tamas organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Department of Medical Physics and Informatics, University of Szeged, Theoretical Medicine Doctoral School, University of Szeged – sequence: 2 givenname: Priya surname: Balasubramanian fullname: Balasubramanian, Priya organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center – sequence: 3 givenname: Marta Noa surname: Valcarcel-Ares fullname: Valcarcel-Ares, Marta Noa organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center – sequence: 4 givenname: Stefano surname: Tarantini fullname: Tarantini, Stefano organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center – sequence: 5 givenname: Andriy surname: Yabluchanskiy fullname: Yabluchanskiy, Andriy organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center – sequence: 6 givenname: Tamas surname: Csipo fullname: Csipo, Tamas organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Department of Medical Physics and Informatics, University of Szeged – sequence: 7 givenname: Agnes surname: Lipecz fullname: Lipecz, Agnes organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Department of Medical Physics and Informatics, University of Szeged – sequence: 8 givenname: Dora surname: Reglodi fullname: Reglodi, Dora organization: Department of Anatomy, MTA-PTE PACAP Research Team, University of Pecs Medical School – sequence: 9 givenname: Xin A. surname: Zhang fullname: Zhang, Xin A. organization: Department of Physiology, University of Oklahoma Health Sciences Center – sequence: 10 givenname: Ferenc surname: Bari fullname: Bari, Ferenc organization: Department of Medical Physics and Informatics, University of Szeged, Theoretical Medicine Doctoral School, University of Szeged – sequence: 11 givenname: Eszter surname: Farkas fullname: Farkas, Eszter organization: Department of Medical Physics and Informatics, University of Szeged, Theoretical Medicine Doctoral School, University of Szeged – sequence: 12 givenname: Anna surname: Csiszar fullname: Csiszar, Anna organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Department of Medical Physics and Informatics, University of Szeged, Theoretical Medicine Doctoral School, University of Szeged – sequence: 13 givenname: Zoltan orcidid: 0000-0002-6035-6039 surname: Ungvari fullname: Ungvari, Zoltan email: zoltan-ungvari@ouhsc.edu organization: Vascular Cognitive Impairment and Neurodegeneration Program, Reynolds Oklahoma Center on Aging, Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Department of Medical Physics and Informatics, University of Szeged, Theoretical Medicine Doctoral School, University of Szeged, Department of Public Health, Semmelweis University, Department of Health Promotion Sciences, the Hudson College of Public Health, University of Oklahoma Health Sciences Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31144244$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Aging Aging - physiology Angiogenesis Animals Biomedical and Life Sciences Brain - blood supply Cell Biology Cell Movement - physiology Cell proliferation Cell Proliferation - physiology Cerebral blood flow Cognitive ability Cognitive Dysfunction - prevention & control Dementia disorders Endothelial cells Endothelial Cells - physiology Endothelium Geriatrics Geriatrics/Gerontology Hydrogen peroxide Hydrogen Peroxide - metabolism Life Sciences Microvessels - cytology Molecular Medicine NAD Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Nicotinamide Nicotinamide Mononucleotide - pharmacology Original Original Article Oxidative stress Oxidative Stress - drug effects Rats, Inbred BN Rats, Inbred F344 SIRT1 protein Vascular dementia Vasodilation Wound healing |
| Title | Nicotinamide mononucleotide (NMN) treatment attenuates oxidative stress and rescues angiogenic capacity in aged cerebromicrovascular endothelial cells: a potential mechanism for the prevention of vascular cognitive impairment |
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