Mechanical signalling among cells and tissues has been shown to be an important, albeit lesser known, form of transducing pathological stimuli. Cytoskeletal (CSK) structures are organized in accordance with tensegrity architecture and, as such, can bear mechanical loads. Vibroacoustic disease (VAD) is a systemic pathology characterized by the abnormal proliferation of extra-cellular matrices (ECM) in the absence of an inflammatory process. The goal of this report is to qualitatively analyse the images obtained from vibroacoustic disease (VAD) pericardial fragments within the context of tensegrity structures.
Drawing upon the numerous scanning and transmission electron microscopy images of VAD patients’ parietal pericardium, which is abnormally thickened and discloses mechanical cell death in all layers. The abnormal thickening is due to the splitting of the fibrosa layer into two halves and, in between, the neo-formation of a loose tissue layer. The internal fibrosa layer follows the systolic and diastolic movements very closely while the external layer does not. The implications of these situations for CSK and ECM mechanotransduction are qualitatively analysed.
The new pericardial structure, composed of five layers instead of three (due to fibrosa splitting and neo-formation of loose tissue layer) is reminiscent of a pneumatic structure. The wave length of the wavy collagen fibres found in the internal fibrosa seem to be more variable than that found in the external fibrosa. The loose tissue layer contains adipose tissue that, due to its viscoelastic properties, can attenuate external mechanical forces. In the meseothelial layer, there is a reinforcement of cell-cell connections, through an increased amount of desmosomes. No hemidesmosomes were identified, however the boundary between mesothelial layer and lower basal lamina exhibits unusual connection, reminiscent of anti-sesmic structures.
Tensegrity architecture of cells and tissue can greatly contribute to the understanding of the biological response to LFN-exposure.
It is probable that pharmacological solutions for LFN-induced pathology targeting CSK and ECM tension would be most successful.
Mariana Alves-Pereira, None.