This approach confirmed a significant upregulation of collagen type IV α2 (30-fold,
P < 0.0001), collagen type V α1 (17-fold,
P < 0.0001), collagen type VI α1 (4-fold,
P < 0.02), and versican (6-fold,
P < 0.0001) in FCD as compared to controls (
Table 3). However, these genes were also upregulated to the same or to an even higher extent in PBK specimens (3- to 160-fold,
P < 0.001 to
P < 0.05) as compared to controls, possibly reflecting a nonspecific endothelial dysfunction. In contrast, agrin (6-fold,
P < 0.001), clusterin (3-fold,
P = 0.002), collagen type I α1 (18-fold,
P = 0.008), collagen type III α1 (13-fold,
P = 0.04), collagen type XVI α1 (8-fold,
P = 0.03), fibronectin 1 (6-fold,
P < 0.001), integrin α4 (4-fold,
P < 0.005), and TGFBI (3-fold,
P = 0.006) displayed a FCD-specific upregulation as compared to both PBK and control specimens (
Table 3;
Fig. 1). Collagen type VIII α2 and fibulin-2 displayed no differential expression in FCD, PBK, and control specimens.