Metabolic profiling of human endothelial cells during autophagy assessed in a biomimetic microfluidic device model

Abstract

Aims: Autophagy is critical to endothelial function. We explored the effects of autophagy induced by serum deprivation on Human Umbilical Vascular Endothelial Cells (HUVEC) metabolome profile and its inhibition by the antimalarial drug chloroquine (CLQ) using a microfluidic biomimetic model.

Main methods: The metabolites secreted by HUVEC into the circulating microfluidics were determined by liquid chromatography mass spectrometry (LC-MS) and further analyzed using Metaboanalyst 3.0 multivariate and pathway analysis tools.

Key findings: Principal component analysis showed the discrimination of metabolites between treated and control groups. The results also identified alterations in metabolites relevant to endothelial function such as arginine, glutamate and energy metabolism pathways. Interestingly, CLQ mostly reversed the changes induced by serum deprivation.

Significance: The knowledge of endothelial metabolic profile during autophagy may contribute to the identification of clinical biomarkers and potential therapeutic approaches based on the regulation of autophagy.

Keywords: Autophagy; Chloroquine; Endothelial dysfunction; HUVEC; Mass spectrometry; Metabolome; Microfluids.