Heat shock protein 90 is downregulated in calcific aortic valve disease

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BMC Cardiovascular Disorders. 2019 Dec 19;19(1):306

Title: Heat shock protein 90 is downregulated in calcific aortic valve disease
Author: Weisell, Jonna; Ohukainen, Pauli; Näpänkangas, Juha; Ohlmeier, Steffen; Bergmann, Ulrich; Peltonen, Tuomas; Taskinen, Panu; Ruskoaho, Heikki; Rysä, Jaana
Publisher: BioMed Central
Date: 2019-12-19
Language: en
URI: http://hdl.handle.net/10138/308713
Abstract: Abstract Background 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. Methods 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. Results 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. Conclusions We describe here a novel data set of proteomic changes associated with CAVD, including downregulation of the pro-inflammatory cytosolic protein, HSP90.
Subject: Aortic valve stenosis
Calcified aortic valve disease
Heat-shock protein

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