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. 2021 Dec 7;3:41–47. doi: 10.1016/j.jvssci.2021.11.002

Fig 3.

Fig 3

A, Carotid tissue isolated from control carotid artery and asymptomatic (Asympt.) and symptomatic (Sympt.) carotid artery plaque. Fluorescence in situ hybridization of nine specimens (three control, three asymptomatic, three symptomatic) showing similar expression of HDAC9 mRNA in human carotid tissue with and without disease but significantly increased protein levels of HDAC9 in diseased carotid tissue. B, Transmission electron microscopy showing striking phenotypic differences in vascular smooth muscle cells (VSMCs) from patients without and with carotid atherosclerosis. Consistent organization was found for actin and cell morphology in the control tissue. Diseased tissue displayed cells with large vacuoles and disorganized morphology. Localization of HDAC9 was found in the electron dense areas of the nucleus and clustering of LGALS3 in the cell cytoplasm of the diseased carotid tissue, which was absent in the control tissue. Samples from three control patients and three patients with symptomatic plaques were analyzed, with representative images shown. Chrom, Chromatin; Cyto, cytoplasm; Memb, membrane; Nu, nucleus.