Quiescin sulfhydryl oxidase (QSOX) is expressed in the human atheroma core: possible role in apoptosis |
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Authors: | Claudia R de Andrade Beatriz S Stolf Victor Debbas Daniela S Rosa Jorge Kalil Veronica Coelho Francisco R M Laurindo |
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Institution: | 1.Vascular Biology Laboratory, Heart Institute (InCor),University of S?o Paulo School of Medicine,S?o Paulo,Brazil;2.Biology of Reproduction Laboratory, Department of Animal Science,Federal University of Ceara (UFC),Fortaleza,Brazil;3.Laboratory of Immunology, Heart Institute (InCor), Medical School,University of S?o Paulo,S?o Paulo,Brazil;4.Institute of Biomedical Sciences,University of S?o Paulo,S?o Paulo,Brazil;5.Laboratory of Clinical Immunology and Allergy (LIM-60), Department of Clinical Medicine,University of S?o Paulo,S?o Paulo,Brazil;6.INCT–Institute for Investigation in Immunology–National Institute of Science and Technology,S?o Paulo,Brazil |
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Abstract: | Quiescin sulfhydryl oxidases (QSOXs) catalyze the formation of disulfide bonds in peptides and proteins, and in vertebrates
comprise two proteins: QSOX1 and QSOX2. QSOX1, the most extensively studied type, has been implicated in protein folding,
production of extracellular matrix, redox regulation, protection from apoptosis, angiogenesis, and cell differentiation. Atherosclerosis
is an immunopathological condition in which redox processes, apoptosis, cell differentiation, and matrix secretion/maturation
have critical roles. Considering these data, we hypothesized that QSOX1 could be involved in this disease, possibly reducing
apoptosis and angiogenesis inside the plaque. QSOX1 labeling in normal human carotid vessels showed predominant expression
by endothelium, subendothelium, and adventitia. In atherosclerotic plaques, however, QSOX1 was highly expressed in macrophages
at the lipid core. QSOX1 expression was also studied in terms of mRNA and protein in cell types present in plaques under apoptotic
or activating stimuli, emulating conditions found in the atherosclerotic process. QSOX1 mRNA increased in endothelial cells
and macrophages after the induction of apoptosis. At the protein level, the correlation between apoptosis and QSOX1 expression
was not evident in all cell types, possibly because of a rapid secretion of QSOX1. Our results propose for the first time
possible roles for QSOX1 in atherosclerosis, being upregulated in endothelial cells and macrophages by apoptosis and cell
activation, and possibly controlling these processes, as well as angiogenesis. The quantitative differences in QSOX1 induction
may depend on the cell type and also on local factors. |
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