Document Detail


Increased CCT-eta expression is a marker of latent and active disease and a modulator of fibroblast contractility in Dupuytren's contracture.
MedLine Citation:
PMID:  23292503     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Latha Satish; David B O'Gorman; Sandra Johnson; Christina Raykha; Bing Siang Gan; James H-C Wang; Sandeep Kathju
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2013-01-06
Journal Detail:
Title:  Cell stress & chaperones     Volume:  18     ISSN:  1466-1268     ISO Abbreviation:  Cell Stress Chaperones     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-06-14     Completed Date:  2013-12-30     Revised Date:  2014-06-18    
Medline Journal Info:
Nlm Unique ID:  9610925     Medline TA:  Cell Stress Chaperones     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  397-404     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism
Biological Markers / metabolism
Cells, Cultured
Chaperonin Containing TCP-1 / antagonists & inhibitors,  genetics,  metabolism*
Dupuytren Contracture / metabolism,  pathology
Fascia / cytology
Fibroblasts / cytology,  physiology*
Humans
Muscle Contraction / physiology
RNA Interference
RNA, Small Interfering / metabolism
Grant Support
ID/Acronym/Agency:
AR049921/AR/NIAMS NIH HHS; AR06139/AR/NIAMS NIH HHS; R01 AR061395/AR/NIAMS NIH HHS; R21 AR060920/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/ACTA2 protein, human; 0/Actins; 0/Biological Markers; 0/RNA, Small Interfering; EC 3.6.1.-/Chaperonin Containing TCP-1
Comments/Corrections

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