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http://purl.uniprot.org/citations/20873970http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20873970http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Our previous proteomic research has indicated that some cytoskeleton proteins show differential expression between thoracic aortic dissection and normal control groups, which suggests a possible mechanism involved in the pathogenesis of the vascular remodeling of this disease. This study was to investigate the expression of these cytoskeleton proteins and their possible molecular pathway in the remodeling process of thoracic aortic dissection.

Methods

Ascending aortic segments were obtained from thoracic aortic dissection patients (Debakey type I, n = 13) and age-matched normal donors (n = 8). Quantitative differences of Destrin, cofilin, and LIM protein kinases (LIMK) were investigated using RT-PCR and Western blot analysis. The relationships between the expression of these proteins and clinical parameters such as age, hypertension and maximal aortic diameter of the patients were analysed statistically.

Results

Western blotting showed that the protein expression of cofilin and LIMK was significantly decreased in thoracic aortic dissection tissue compared with normal control, (p = 0.004 for cofilin, p < 0.001 for LIMK). The mRNA levels of cofilin and LIMK were lower in thoracic aortic dissection than normal control and were coincident with the protein expression (p = 0.0039 for cofilin, p = 0.017 for LIMK). A significant correlation (Spearman's rho = -0.521, p = 0.019) was found between LIMK protein expression and maximal aortic diameter; lower levels of LIMK expression were associated with larger aortic diameters.

Conclusions

Changes in the expression of cytoskeletal regulatory proteins such as LIMK and cofilin may play a role in weakening thoracic aortic medial tissue, as a precondition to thoracic aortic dissection."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.org/dc/terms/identifier"doi:10.3109/00365513.2010.521572"xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/author"Tian L."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/author"Lu Q.S."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/author"Jing Z.P."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/author"Liao M.F."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/name"Scand J Clin Lab Invest"xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/pages"523-528"xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/title"A study of the expression and interaction of Destrin, cofilin, and LIMK in Debakey I type thoracic aortic dissection tissue."xsd:string
http://purl.uniprot.org/citations/20873970http://purl.uniprot.org/core/volume"70"xsd:string
http://purl.uniprot.org/citations/20873970http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20873970
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