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DOI: 10.1055/s-0035-1544497
Effects of Chronic Atrial Fibrillation on the Structural Remodeling Processes in Human Patients
Objectives: Atrial fibrillation (AF) is the most common arrhythmia worldwide. It is associated with structural and electrical remodelling processes of the cardiac tissue, which maintain the disease. Expression and membrane density of several proteins is known to be altered. Thus, we investigated possible changes of the cell organelle Golgi apparatus and the formation of cytoskeletal α- tubulin as the pathways of protein trafficking.
Methods: Human specimens were collected during cardiac surgery. A total of 18 atrial samples of sinus rhythm (SR) and 17 atrial samples of chronic AF were stained by immunofluorescence to analyze the Golgi apparatus based on fluorescence signal intensity as well as the number and size of vesicular components in both groups. Furthermore, α- tubulin filaments with a length of at least 10µm were quantified for SR and AF tissue.
Results: In healthy SR samples the Golgi apparatus was found at the poles of the nucleus with a significant (p < 0,05) increase in size per area of the cell compared with AF samples (0.003 ± 0.0003 versus 0.0009 ± 0.0002,respectively). For AF diseased tissue many, small and diffused fragments distributed over the whole cell were detected. The SR cardiomyocytes exhibited significantly less components of the Golgi apparatus (24.1 ± 1.6 versus 57.3 ± 2.7, p < 0,05) and resulted in a significantly lower fluorescence intensity lateral of the nucleus than AF cells (0.71 ± 0.03 versus 0.86 ± 0.03, p < 0,05). Additionally, α- tubulin in healthy tissue was found in long and stabilized filaments in contrast to patients with AF exhibiting short and fractionated elements.
Conclusion: Interestingly AF induces a fragmentation of the Golgi apparatus (see Fig. 1) and consequently a depolymerisation of α- tubulin. Therefore, the directed intracellular transport of proteins could break down. This may cause a restructuring and reorganization in the cardiomyocytes. Thus, AF results in changes of the protein trafficking pathways.
Fig. 1 SR(A), AF (B), red: golgi apparatus, green: α- tubulin, blue: nucleus.