Abstract
β-Galactosidase (β-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 β-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 β-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 β-Gal activity in young and senescent endothelial cells (HUVECs) cultured in normo- and hyper-glycaemic environment.A significant age-related increase of plasmatic β-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.β-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 β-Gal activity in milieu compared to normo-glycaemic condition.Overall our data reinforce the notion that plasmatic β-Gal activity could be a systemic biomarker of aging, whereas T2DM patients are characterized by a different age-releated trend.
Highlights
The human lysosomal enzyme β-D-galactosidase (β-Gal) is an exoglycosidase that catalyzes the hydrolysis of terminal β-linked galactose residues in glycoproteins, glycolipids and proteoglycans [1]
The anthropometric and biochemical parameters of 230 healthy subjects, defined as control subjects (CTR) and 230 patients affected by T2DM were reported in Table 1A and 1B, respectively
The relevance of our result is related to the evidence that the delaying of senescent cell accumulation or the reduction of senescent cell burden is associated with delay, prevention, or alleviation of multiple senescence-associated conditions and age-related diseases (ARDs) [31]
Summary
The human lysosomal enzyme β-D-galactosidase (β-Gal) is an exoglycosidase that catalyzes the hydrolysis of terminal β-linked galactose residues in glycoproteins, glycolipids and proteoglycans [1]. In the past little attention was paid to glycohydrolases present in cellular compartments different from lysosomes, growing evidence suggested the presence of active lysosomal enzymes in extra-lysosomal compartments, such as the plasma membrane [12] and the extracellular environment [13]. Autophagolysosomes and their content instead of being fully processed by degradation can be extruded from cells through unconventional secretion mechanisms, including the so called “secretory autophagy” [14, 15]. It was hypothesized that plasmatic β-Gal activity might be a manifestation of “systemic senescence status” in the course of ARDs [25]
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