Abstract
Calcific aortic valve and coronary artery diseases are related cardiovascular pathologies in which common processes lead to the calcification of the corresponding affected tissue. Among the mechanisms involved in calcification, the oxidative stress that drives the oxidation of sulfur-containing amino acids such ascysteines is of particular interest. However, there are important differences between calcific aortic valve disease and coronary artery disease, particularly in terms of the reactive oxygen substances and enzymes involved. To evaluate what effect coronary artery disease has on aortic valves, we analyzed valve tissue from patients with severe calcific aortic stenosis with and without coronary artery disease. Proteins and peptides with oxidized cysteines sites were quantified, leading to the identification of 16 proteins with different levels of expression between the two conditions studied, as well as differences in the redox state of the tissue. We also identified two specific sites of cysteine oxidation in albumin that have not been described previously. These results provide evidence that coronary artery disease affects valve calcification, modifying the molecular profile of aortic valve tissue. In addition, the redox proteome is also altered when these conditions coincide, notably affecting human serum albumin.
Highlights
We set out to study the effect of coronary artery disease (CAD) on the calcification of the aortic valve (AV) in CAVD using a high-throughput proteomic procedure based on the filter-aided stable isotope labeling of oxidized Cys (FASILOX) technique
By analyzing the proteome of the AV tissue obtained from these participants, we identified a total of 6353 peptides that corresponded to 1562 unique proteins in at least 90% of the samples
We identified 16 proteins that displayed differences in expression above 50% between the two study groups: lumican (LUM); decorin (DCN); collagen alpha-1(XV) chain (COFA1); biglycan (BGN); plasma protease C1 inhibitor (IC1); sex hormone-binding globulin (SHBG); inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4); Ig mu chain C region (IGHM); zinc-alpha-2-glycoprotein (ZA2G); coagulation factor IX
Summary
Calcific aortic valve disease (CAVD) or aortic valve (AV) stenosis is a progressive condition in which a narrowing of the AV area occurs due to a thickening and calcification of the leaflets, the progression of which is associated with worse outcomes [1,2,3]. AV degeneration shows several similarities with coronary atherosclerosis, even sharing many clinical risk factors [4]. The presence of coronary artery disease (CAD) is a negative predictive indicator in patients with CAVD [5,6,7] and it is recommended that coronary arteries are evaluated by invasive coronary angiography or coronary computed tomography (CT) angiography prior to the prescription of surgical or transcatheter AV replacement [2].
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