Published February 26, 2020 | Version v1
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Dataset related to the article "Pro-oxidant and pro-inflammatory effects of glycated albumin on cardiomyocytes"

  • 1. Centro Cardiologico Monzino, IRCCS, Milan, Italy
  • 2. epartment of Pharmaceutical Sciences, University of Milan, Milan, Italy
  • 3. Centro Cardiologico Monzino, IRCCS, Milan, Italy and Centro Cardiologico Monzino, IRCCS, Milan, Italy
  • 4. Department of Pharmaceutical Sciences, University of Milan, Milan, Italy
  • 5. entro Cardiologico Monzino, IRCCS, Milan, Italy

Description

This record contains raw data related to the article "Pro-oxidant and pro-inflammatory effects of glycated albumin on cardiomyocytes"

A B S T R A C T
Human serum albumin (HSA) is the most abundant circulating protein in the body and presents an extensive range of biological functions. As such, it is prone to undergo post-translational modifications (PTMs). The nonenzymatic early glycation of HSA, one of the several PTMs undergone by HSA, arises from the addition of reducing sugars to amine group residues, thus modifying the structure of HSA. These changes may affect HSA functions impairing its biological activity, finally leading to cell damage.
The aim of this study was to quantitate glycated-HSA (GA) levels in the plasma of heart failure (HF) patients and to evaluate the biological effects of GA on HL-1 cardiomyocytes.
Plasma GA content from HF patients and healthy subjects was measured by direct infusion electrospray ionization mass spectrometry (ESI-MS). Results pointed out a significant increase of GA in HF patients with respect to the control group (p < 0.05). Additionally, after stimulation with GA, proteomic analysis of HL-1 secreted proteins showed the modulation of several proteins involved, among other processes, in the response to stress. Further, stimulated cells showed a rapid increase in ROS generation, higher mRNA levels of the inflammatory cytokine interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and higher levels of the oxidative 4-HNE-protein adducts and carbonylated proteins.
Our findings show that plasma GA is increased in HF patients. Further, GA exerts pro-inflammatory and prooxidant effects on cardiomyocytes, which suggest a causal role in the etiopathogenesis of HF.

Notes

This work was supported by the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie (grant agreement number 675132) and by the Italian Ministry of Health, Rome, Italy (Ricerca Corrente 2017 BIO 18, ID 2631209).

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Additional details

Related works

Is supplement to
Journal article: 10.1016/j.freeradbiomed.2019.06.023 (DOI)

Funding

European Commission
MASSTRPLAN - MASS Spectrometry TRaining network for Protein Lipid adduct ANalysis 675132