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   <subfield code="a">Increased CCT-eta expression is a marker of latent and active disease and a modulator of fibroblast contractility in Dupuytren's contracture</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Latha Satish, David O'Gorman, Sandra Johnson, Christina Raykha, Bing Gan, James Wang, Sandeep Kathju]</subfield>
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   <subfield code="a">Dupuytren's contracture (DC) is a fibroproliferative disorder of unknown etiology characterized by a scar-like contracture that develops in the palm and/or digits. We have previously reported that the eta subunit of the chaperonin containing T-complex polypeptide (CCT-eta) is increased in fibrotic wound healing, and is essential for the accumulation of α-smooth muscle actin (α-SMA) in fibroblasts. The purpose of this study was to determine if CCT-eta is similarly implicated in the aberrant fibrosis seen in DC and to investigate the role of CCT-eta in the behavior of myo/fibroblasts in DC. Fibroblasts were obtained from DC-affected palmar fascia, from adjacent phenotypically normal palmar fascia in the same DC patients (PF), and from non-DC palmar fascial tissues in patients undergoing carpal tunnel (CT) release. Inherent contractility in these three populations was examined using fibroblast-populated collagen lattices (FPCLs) and by cell traction force microscopy. Expression of CCT-eta and α-SMA protein was determined by Western blot. The effect of CCT-eta inhibition on the contractility of DC cells was determined by deploying an siRNA versus CCT-eta. DC cells were significantly more contractile than both matching palmar fascial (PF) cells and CT cells in both assays, with PF cells demonstrating an intermediate contractility in the FPCL assay. Whereas α-SMA protein was significantly increased only in DC cells compared to PF and CT cells, CCT-eta protein was significantly increased in both PF and DC cells compared to CT cells. siRNA-mediated depletion of CCT-eta inhibited the accumulation of both CCT-eta and α-SMA protein in DC cells, and also significantly decreased the contractility of treated DC cells. These observations suggest that increased expression of CCT-eta appears to be a marker for latent and active disease in these patients and to be essential for the increased contractility exhibited by these fibroblasts.</subfield>
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   <subfield code="a">Cell Stress Society International, 2013</subfield>
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   <subfield code="a">Dupuytren's contracture</subfield>
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   <subfield code="a">Satish</subfield>
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   <subfield code="u">Department of Plastic Surgery, University of Pittsburgh, 15213, Pittsburgh, PA, USA</subfield>
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   <subfield code="a">O'Gorman</subfield>
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   <subfield code="a">Raykha</subfield>
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   <subfield code="t">Cell Stress and Chaperones</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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