Multi-scale measurement of artery wall deformation to study hypertrophy mechanism in hypertension

Abstract

As one of the mechanotransduction pathways, it has been suggested that load applied to tissue may deform cells in the tissue, nuclei in the cells, and then chromatin in the nuclei, and this may affect mRNA transcription. In this study, we have been studying how the deformation applied to artery wall is transferred to smooth muscle cells, nuclei, and finally chromatin to elucidate the mechanism of wall hypertrophy during hypertension. We measured microscopic deformation of thin-sliced rabbit thoracic aortas during tensile test and confirmed that the deformation was complex and heterogeneous and elongation of the nuclei was 40-50% smaller than that of the tissue. We also found that the shape and chromatin distribution of the nucleus changed drastically in artery tissue cultured in no load condition. It is suggested that nuclear deformation is different from tissue deformation and the nuclear morphology changes depending on their mechanical environment.