Abstract
Aggregated low density lipoproteins (agLDL) contribute to massive intracellular cholesteryl ester (CE) accumulation in human vascular smooth muscle cells (VSMC). Our aim was to determine the conformational and physical structure of agLDL and elastic material produced either by control human VSMC or by agLDL-loaded human VSMC (agLDL-VSMC). At the conformational level scanned by FTIR spectroscopy, a new undefined, probably non-H-bonded, structure for tropoelastin produced by agLDL-VSMC is revealed. By differential scanning calorimetry, a decrease of water affinity and a drop of the glass transition associated with aggregated tropoelastin (from 200°C to 159°C) in the supernatant from agLDL VSMC are evidenced. This second phenomenon is due to an interaction between agLDL and tropoelastin as detected by the weak specific FTIR absorption band of agLDL in supernatant from agLDL-loaded VSMC.
Highlights
vascular smooth muscle cells (VSMC) in atherosclerotic lesion are unable to produce normal elastic fibers due to atherosclerotic risk factors such as diabetes and associated hyperglycemia, endothelial dysfunction, and inflammation [1, 2]
Intracellular cholesterol accumulation alters proteoglycan composition [9] and collagen assembly [10] in VSMC, but it is unknown whether intracellular lipid may change the physical characteristics of the tropoelastin synthesized by human VSMC
A slight shoulder at 1734 cm−1 in the spectrum of the supernatant from aggregation of LDLs (agLDL)-VSMC is indicative of a weak fraction of agLDL in the sample that could remain after the purification, suggesting an interaction between tropoelastin and agLDL, as previously reported for tropoelastin and LDL [18]
Summary
VSMC in atherosclerotic lesion are unable to produce normal elastic fibers due to atherosclerotic risk factors such as diabetes and associated hyperglycemia, endothelial dysfunction, and inflammation [1, 2]. VSMC become foam cells through the uptake of diversely modified LDLs [5, 6], whereas the aggregation of LDLs (agLDL) seems to be a key condition for lipid accumulation in VSMCs [7, 8]. Intracellular cholesterol accumulation alters proteoglycan composition [9] and collagen assembly [10] in VSMC, but it is unknown whether intracellular lipid may change the physical characteristics of the tropoelastin synthesized by human VSMC. The aim of this work was to characterize agLDL as well as tropoelastin produced by agLDL-lipid-loaded human VSMC versus that produced by control VSMC using polymer characterization techniques that were previously shown to be efficient in checking the molecular architecture and chain dynamics of proteins [11, 12]
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