Heat shock protein 90 is downregulated in calcific aortic valve disease

Calcific aortic valve disease (CAVD) is an atheroinflammatory process; finally it leads to progressive calcification of the valve. There is no effective pharmacological treatment for CAVD and many of the underlying molecular mechanisms remain unknown. We conducted a proteomic study to reveal novel f...

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Published inBMC cardiovascular disorders Vol. 19; no. 1; p. 306
Main Authors Weisell, Jonna, Ohukainen, Pauli, Näpänkangas, Juha, Ohlmeier, Steffen, Bergmann, Ulrich, Peltonen, Tuomas, Taskinen, Panu, Ruskoaho, Heikki, Rysä, Jaana
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 19.12.2019
BioMed Central
BMC
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Summary:Calcific aortic valve disease (CAVD) is an atheroinflammatory process; finally it leads to progressive calcification of the valve. There is no effective pharmacological treatment for CAVD and many of the underlying molecular mechanisms remain unknown. We conducted a proteomic study to reveal novel factors associated with CAVD. We compared aortic valves from patients undergoing valvular replacement surgery due to non-calcified aortic insufficiency (control group, n = 5) to a stenotic group (n = 7) using two-dimensional difference gel electrophoresis (2D-DIGE). Protein spots were identified with mass spectrometry. Western blot and immunohistochemistry were used to validate the results in a separate patient cohort and Ingenuity Pathway Analysis (IPA) was exploited to predict the regulatory network of CAVD. We detected an upregulation of complement 9 (C9), serum amyloid P-component (APCS) and transgelin as well as downregulation of heat shock protein (HSP90), protein disulfide isomerase A3 (PDIA3), annexin A2 (ANXA2) and galectin-1 in patients with aortic valve stenosis. The decreased protein expression of HSP90 was confirmed with Western blot. We describe here a novel data set of proteomic changes associated with CAVD, including downregulation of the pro-inflammatory cytosolic protein, HSP90.
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ISSN:1471-2261
1471-2261
DOI:10.1186/s12872-019-01294-2