Journal
ONCOTARGET
Volume 8, Issue 55, Pages 93338-93348Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.21848
Keywords
cellular senescence; beta galactosidase activity; type 2 diabetes; aging; inflammaging; Gerotarget
Categories
Funding
- Universita Politecnica delle Marche, Italy, RSA
- Universita Politecnica delle Marche, Italy, MIRAGE project
- Umberto Veronesi Foundation
Ask authors/readers for more resources
beta-Galactosidase (beta-Gal) activity has been the most extensively utilized biomarker for the detection of cellular senescence. It can be measured also in plasma, and few recent evidence showed an altered plasmatic beta-Gal activity in patients affected by some age-related diseases (ARDs). Since T2DM is one of the most common ARDs, we aimed to investigate if plasmatic beta-Gal activity is modulated in T2DM patients and if age could affect such modulation. To gain mechanistic insights we paralleled this investigation with the evaluation of beta-Gal activity in young and senescent endothelial cells (HUVECs) cultured in normo- and hyper-glycaemic environment. A significant age-related increase of plasmatic beta-Gal activity was observed in healthy subjects (n. 230; 55-87 years), whereas the enzymatic activity was significantly reduced in T2DM patients (n. 230; 55-96 years) compared to healthy subjects. beta-Gal activity detectable both in cells and in the culture medium was significantly increased in senescent cells compared to the younger ones, both under normo- and hyper-glycaemic condition. However, the hyper-glycaemic condition was not associated with an increased beta-Gal activity in milieu compared to normo-glycaemic condition. Overall our data reinforce the notion that plasmatic beta-Gal activity could be a systemic biomarker of aging, whereas T2DM patients are characterized by a different age-releated trend.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available