Chronic Intermittent Hypoxia Triggers a Senescence-like Phenotype in Human White Preadipocytes.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
22 04 2020
Historique:
received: 21 03 2019
accepted: 03 04 2020
entrez: 24 4 2020
pubmed: 24 4 2020
medline: 25 11 2020
Statut: epublish

Résumé

Obstructive sleep apnea (OSA) is a common sleep disorder associated with obesity. Emerging evidence suggest that OSA increases the risk of cardiovascular morbidity and mortality partly via accelerating the process of cellular aging. Thus, we sought to examine the effects of intermittent hypoxia (IH), a hallmark of OSA, on senescence in human white preadipocytes. We demonstrate that chronic IH is associated with an increased generation of mitochondrial reactive oxygen species along with increased prevalence of cells with nuclear localization of γH2AX & p16. A higher prevalence of cells positive for senescence-associated β-galactosidase activity was also evident with chronic IH exposure. Intervention with aspirin, atorvastatin or renin-angiotensin system (RAS) inhibitors effectively attenuated IH-mediated senescence-like phenotype. Importantly, the validity of in vitro findings was confirmed by examination of the subcutaneous abdominal adipose tissue which showed that OSA patients had a significantly higher percentage of cells with nuclear localization of γH2AX & p16 than non-OSA individuals (20.1 ± 10.8% vs. 10.3 ± 2.7%, P

Identifiants

pubmed: 32321999
doi: 10.1038/s41598-020-63761-7
pii: 10.1038/s41598-020-63761-7
pmc: PMC7176724
doi:

Substances chimiques

CDKN2A protein, human 0
Cyclin-Dependent Kinase Inhibitor p16 0
H2AX protein, human 0
Histones 0
Reactive Oxygen Species 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

6846

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL065176
Pays : United States

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Auteurs

Katarzyna Polonis (K)

Department of Cardiovascular Medicine, Mayo Clinic, MN, Rochester, USA.

Christiane Becari (C)

Department of Cardiovascular Medicine, Mayo Clinic, MN, Rochester, USA.
Department of Surgery and Anatomy, Ribeirao Preto Medical School, Ribeirão Preto, SP, Brazil.

C Anwar A Chahal (CAA)

Department of Cardiovascular Medicine, Mayo Clinic, MN, Rochester, USA.
Mayo Clinic Graduate School of Biomedical Sciences, MN, Rochester, USA.

Yuebo Zhang (Y)

Department of Cardiovascular Medicine, Mayo Clinic, MN, Rochester, USA.

Alina M Allen (AM)

Division of Gastroenterology and Hepatology, Mayo Clinic, MN, Rochester, USA.

Todd A Kellogg (TA)

Department of Surgery, Mayo Clinic, MN, Rochester, USA.

Virend K Somers (VK)

Department of Cardiovascular Medicine, Mayo Clinic, MN, Rochester, USA.

Prachi Singh (P)

Department of Cardiovascular Medicine, Mayo Clinic, MN, Rochester, USA. prachi.singh@pbrc.edu.
Pennington Biomedical Research Center, LA, Baton Rouge, USA. prachi.singh@pbrc.edu.

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