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Lipid Loading of Human Vascular Smooth Muscle Cells Induces Changes in Tropoelastin Protein Levels and Physical Structure

Samouillan, Valérie and Dandurand, Jany and Nasarre, Laura and Badimon, Lina and Lacabanne, Colette and Llorente-Cortés, Vicenta Lipid Loading of Human Vascular Smooth Muscle Cells Induces Changes in Tropoelastin Protein Levels and Physical Structure. (2012) Biophysical Journal, 103 (3). 532-540. ISSN 0006-3495

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Official URL: http://dx.doi.org/10.1016/j.bpj.2012.06.034


Aggregated low-density lipoprotein (agLDL), one of the main LDL modifications in the arterial intima, contributes to massive intracellular cholesteryl ester (CE) accumulation in human vascular smooth muscle cells (VSMC), which are major producers of elastin in the vascular wall. Our aim was to analyze the levels, physical structure, and molecular mobility of tropoelastin produced by agLDL-loaded human VSMC (agLDL-VSMC) versus that produced by control VSMC. Western blot analysis demonstrated that agLDL reduced VSMC-tropoelastin protein levels by increasing its degradation rate. Moreover, our results demonstrated increased levels of precursor and mature forms of cathepsin S in agLDL-VSMC. Fourier transform infrared analysis revealed modifications in the secondary structures of tropoelastin produced by lipid-loaded VSMCs. Thermal and dielectric analyses showed that agLDL-VSMC tropoelastin has decreased glass transition temperatures and distinct chain dynamics that, in addition to a loss of thermal stability, lead to strong changes in its mechanical properties. In conclusion, agLDL lipid loading of human vascular cells leads to an increase in cathepsin S production concomitantly with a decrease in cellular tropoelastin protein levels and dramatic changes in secreted tropoelastin physical structure. Therefore, VSMC-lipid loading likely determines alterations in the mechanical properties of the vascular wall and plays a crucial role in elastin loss during atherosclerosis.

Item Type:Article
Additional Information:Thanks to the Biophysical Society editor. The definitive version is available at : http://www.sciencedirect.com/science/article/pii/S0006349512007230
HAL Id:hal-03528867
Audience (journal):International peer-reviewed journal
Uncontrolled Keywords:
Institution:French research institutions > Centre National de la Recherche Scientifique - CNRS (FRANCE)
Other partners > Consejo Superior de Investigaciones Científicas - CSIC (SPAIN)
Université de Toulouse > Institut National Polytechnique de Toulouse - Toulouse INP (FRANCE)
Université de Toulouse > Université Toulouse III - Paul Sabatier - UT3 (FRANCE)
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Laboratory name:
Deposited On:13 May 2013 14:22

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