Smooth muscule transgeline and its role the atherosclerotic process

Abstract

Aim. To study the changes in smooth muscle transgeline in atherosclerotic lesions of thoracic aorta using
proteomic technologies.

Materials and methods. The study material was autopsy samples of thoracic aorta obtained within 1 day after death (n = 22). To identify autoantigens, the blood serum of men with initial and advanced atherosclerosis was used (n = 27). To study proteins, O'Farrell two-dimensional electrophoresis, NEPHGE, IEF modifications, time-of-flight and tandem MALDI-TOF mass spectrometry were used.
Results. When studying autopsy tissues in the series normal tissue-lipid stain/strip – lipofibrotic plaque, an increase of the transgelin protein fraction encoded by the TAGLN gene was revealed, depending on the aggravation of the atherosclerotic process from the absence or trace amount in samples without ath-erosclerosis to the detection of various isoforms at the fibrotic stage plaque. Moreover, partially oxidized TAGLN fragments were detected, which is characteristic of many proteins during atherogenesis, but was first detected for transgeline.
In immunoblotting the blood serum of patients with severe atherosclerosis gave a reaction to transgeline as an autoantigen, and there was no reaction of blood serum in the group with initial atherosclerosis. In addition, a significant correlation was found between the serum response to transgeline and the level of mono-CRP in the group with severe atherosclerosis.
Conclusions. The results showed that smooth muscle transgeline is possibly a component of the pathogenesis of atherosclerosis and its progression. The presence of autoantibodies to smooth muscle trans-geline was detected in the blood serum of some patients with severe atherosclerosis, and its association with mono-CRP may indicate the involvement of both an inflammatory and immune response in the pathogenesis of atherosclerosis.