A study of the expression and interaction of Destrin, cofilin, and LIMK in Debakey I type thoracic aortic dissection tissue

Abstract

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.

Key Words::

• Aortic diameter
• cofilin
• Destrin
• gene
• LIMK
• protein
• thoracic aortic dissection

Acknowledgement

This work was supported by National Natural Science Foundation of China (30600599 and 81070253).

Funding: This work was supported by the National Natural Science Foundation of China (30600599 and 81070253).

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.