Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 136, Issue 9, Pages 1792-1800Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2016.05.113
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Funding
- NIAMS NIH HHS [K08 AR060802, R01 AR063611, R01 AR065183, R01 AR042742, R01 AR054966, K01 AR059678, R01 AR050511] Funding Source: Medline
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In a transcriptome study of lesional psoriatic skin (PP) versus normal skin, we found a coexpressed gene module (N5) enriched 11.5-fold for lipid biosynthetic genes. We also observed fewer visible hairs in PP skin, compared with uninvolved nonlesional psoriatic skin or normal skin (P < 0.0001). To ask whether these findings might be due to abnormalities of the pilosebaceous unit, we carried out three-dimensional morphometric analysis of paired PP and nonlesional psoriatic skin biopsies. Sebaceous glands were markedly atrophic in PP versus nonlesional psoriatic skin (91% average reduction in volume, P = 0.031). Module N5 genes were strongly downregulated in PP versus normal skin (fold change < 0.25, 44.4-fold) and strongly upregulated in sebaceous hyperplasia (fold change > 4, 54.1-fold). The intersection of PP-downregulated and sebaceous hyperplasia-upregulated gene lists generated a gene expression signature consisting solely of module N5 genes, whose expression in PP versus normal skin was inversely correlated with the signature of IL17-stimulated keratinocytes. Despite loss of visible hairs, morphometry identified elongated follicles in PP versus nonlesional psoriatic skin (average 1.7 vs. 1.2 mm, P = 0.020). These results document sebaceous gland atrophy in nonscalp psoriasis, identify a cytokine-regulated set of sebaceous gland signature genes, and suggest that loss of visible hair in PP skin may result from abnormal sebaceous gland function.
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