The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD + decline

Claudia Chini, Kelly A. Hogan, Gina M. Warner, Mariana G. Tarragó, Thais R. Peclat, Tamar Tchkonia, James L Kirkland, Eduardo Nunes Chini

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)486-493
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume513
Issue number2
DOIs
StatePublished - May 28 2019
Externally publishedYes

Fingerprint

NAD+ Nucleosidase
NAD
Cell Aging
Aging of materials
Phenotype
Tissue
Endothelial Cells
Macrophages
Endothelial cells
Chemokines
Bone
Homeostasis
Up-Regulation
Cytokines
Messenger RNA
Enzymes
Proteins

Keywords

  • Aging
  • CD38
  • Inflammaging
  • NAD
  • Senescence

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

The NADase CD38 is induced by factors secreted from senescent cells providing a potential link between senescence and age-related cellular NAD + decline . / Chini, Claudia; Hogan, Kelly A.; Warner, Gina M.; Tarragó, Mariana G.; Peclat, Thais R.; Tchkonia, Tamar; Kirkland, James L; Chini, Eduardo Nunes.

In: Biochemical and Biophysical Research Communications, Vol. 513, No. 2, 28.05.2019, p. 486-493.

Research output: Contribution to journalArticle

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AU - Peclat, Thais R.

AU - Tchkonia, Tamar

AU - Kirkland, James L

AU - Chini, Eduardo Nunes

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N2 - 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.

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