Fig. 6: Hyperglycemia reduces vascular smooth muscle cells migration and differentiation.

a Summary of TGF-β2 effects in the human plaque fibrous-repair process. b Visium spatial deep sequencing on human plaque tissue sections was used to characterize the spatial distribution of the four phenotypes of vascular smooth muscle cells identified by single-cell RNA sequencing in all PTPRC⁻ spots. Cluster 1 (contractile)-red. Cluster 2 (adipocyte-like)-dark blue. Cluster 3 (synthetic/fibroblast-like)- light blue. Cluster 5 (macrophage-like)- white. c The prediction scores to be contractile and macrophage-like vascular smooth muscle cells were lower in plaque caps from patients with type 2 diabetes (T2D, n = 4 patient samples) than patients without diabetes (n = 5 patient samples). Two-sided Student’s t-tests were used. The boxes represent the interquartile range (IQR; 25th to the 75th percentile). The central line within each box marks the median. The whiskers extend from the minimum value, calculated as the lower quartile minus 1.5 times the IQR, to the maximum value, determined as the upper quartile plus 1.5 times the IQR. d Proportions of TGFB2⁻ and TGFB2⁺ spots in plaque caps in relation to patients with or without T2D. e TGF-β2 stimuli induced differentiation of synthetic proliferative human coronary arterial smooth muscle cells with increased expression of contractile marker genes: TAGLN, CALD1 and CNN1. P-values were obtained from one-way repeated measure ANOVA followed by Dunnett post-hoc test (two-sided). Results are expressed as mean ± SEM. n = 9 biological replicates from three independent experiments in each group were used to assess TAGLN and CALDI gene expression. n = 6 biological replicates from three independent experiments were used to measure CNN1 gene expression. Source data are provided in the source data file.