Mechanisms of adipose tissue extracellular matrix alterations in an in vitro model of adipocytes hypoxia and aging.
Adipocytes
/ immunology
Adipose Tissue
/ metabolism
Aging
/ immunology
Caveolins
/ metabolism
Cells, Cultured
Cellular Senescence
/ physiology
Extracellular Matrix
/ immunology
Fibrosis
/ immunology
Humans
Hypoxia
/ immunology
Inflammation
/ immunology
Sirtuin 1
/ metabolism
Tumor Suppressor Protein p53
/ metabolism
Adipocyte
Aging
Caveolin
Fibrosis
Hypoxia
Inflammation
Journal
Mechanisms of ageing and development
ISSN: 1872-6216
Titre abrégé: Mech Ageing Dev
Pays: Ireland
ID NLM: 0347227
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
received:
23
06
2020
revised:
12
09
2020
accepted:
25
09
2020
pubmed:
6
10
2020
medline:
29
10
2021
entrez:
5
10
2020
Statut:
ppublish
Résumé
Fibrosis has been considered as a hallmark of dysfunctional adipose tissue (AT), however the role and mechanisms of fibrosis in the age related AT dysfunction are not yet well characterized. The aim of the study was to investigate the mechanisms of extracellular matrix (ECM) alterations and the role of caveolins, using an in vitro model of adipocyte aging and hypoxia. Hypoxic adipocytes, but also aged adipocytes, were characterized by a significant increase in gene expression of pro-inflammatory cytokines and ECM components. Immunofluorescence analysis confirmed an increase in collagen VI-A3 in hypoxic and also in aged adipocytes. However aged adipocytes were characterized by only a slight increase in HIF1α immunofluorescence and by a more relevant increase in senescence compared to hypoxic and mature adipocytes, with an increase in p-53 protein and a decrease in SIRT 1 protein. Immunofluorescence and western blot analysis revealed a significant decrease in caveolin-1 expression in hypoxic adipocytes and even more in aged adipocytes. In conclusions, aging adipocytes are associated to alteration of ECM and fibrosis, by modulation of the caveolins through complex mechanisms where inflammation, hypoxia and cellular senescence are coexisting.
Identifiants
pubmed: 33017598
pii: S0047-6374(20)30170-6
doi: 10.1016/j.mad.2020.111374
pii:
doi:
Substances chimiques
Caveolins
0
Tumor Suppressor Protein p53
0
SIRT1 protein, human
EC 3.5.1.-
Sirtuin 1
EC 3.5.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
111374Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.