Epidermal barrier alterations in tape-strips compared to
biopsies
We next evaluated DEGs between AD and controls in either tape-strips or
biopsies among a previously published epidermal barrier
gene-subse4,11,30,66 (Figure 4) . While
terminal differentiation (FLG2, SCEL, PSORS1C2, LCE5A) and keratin
(KRT77, KRT79) products were significantly decreased in both techniques,
greater decreases were observed in tape-strips. AKR1C3, which is
expressed by differentiated keratinocytes, was the most down-regulated
gene unique to tape-strips (Figure E1 ). Significant decreases
in gap junction genes (GJB3, GJB5) were only seen in tape-strips
(Figure 4, Table E1 ). Tight junction components like claudins
and cadherins (CLDN8, CDH12)67 were comparably
suppressed in tape-strips and biopsies, while CLDN1 was uniquely
significantly decreased in biopsies. Markers of epidermal
hyperplasia/proliferation (KRT6A, KRT6B, KRT16, KRT17, MKI67, AKR1B10,
AKR1B15) and cornification (SPRR1A, SPRR2C, SPRR3) showed higher or
unique increases in biopsies.
There was considerable variability in lipid biosynthesis and metabolism
genes. PNPLA3, GAL, FA2H, FABP7, DGAT2, ACER1, ORMDL3, and DHCR7 were
significantly decreased in both, with slightly greater FCHs in
tape-strips, and DEGS2 and SPTLC3 were significantly down-regulated only
in tape-strips. However, several other lipid-related genes (ELOVL3,
FAR2, FADS2, ACOX2) were uniquely down-regulated in biopsies. A few
genes (AGPAT3, FADS1, ELOVL5, SOAT1, LPIN1, PPARG) were decreased in
biopsies, but increased in lesional tape-strips.