Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 513, Issue 2, Pages 486-493Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2019.03.199
Keywords
CD38; NAD(+); Aging; Senescence; Inflammaging
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Funding
- Glenn Foundation for Medical Research via the Paul F. Glenn Laboratories for the Biology of Aging at the Mayo Clinic
- National Institutes of Health (NIH) grants from the National Institute of Aging (NIA) [AG-26094, AG-58812]
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Tissue nicotinamide adenine dinucleotide (NAD(+)) decline has been implicated in aging. We have recently identified CD38 as a central regulator involved in tissue NAD(+) decline during the aging process. CD38 is an ecto-enzyme highly expressed in endothelial and inflammatory cells. To date, the mechanisms that regulate CD38 expression in aging tissues characterized by the presence of senescent cells is not completely understood. Cellular senescence has been described as a hallmark of the aging process and these cells are known to secrete several factors including cytokines and chemokines through their senescent associated secretory phenotype (SASP). Here we investigated if the cellular senescence phenotype is involved in the regulation of CD38 expression and its NADase activity. We observed that senescent cells do not have high expression of CD38. However, the SASP factors secreted by senescent cells induced CD38 mRNA and protein expression and increased CD38-NADase activity in non-senescent cells such as endothelial cells or bone marrow derived macrophages. Our data suggest a link between cellular senescence and NAD(+) decline in which SASP-mediated upregulation of CD38 can disrupt cellular NAD(+) homeostasis. (C) 2019 The Authors. Published by Elsevier Inc.
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