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Research Square
By Romeu A.
Abstract Background: Psoriasis is an immune-mediated inflammatory skin disease driven by complex transcriptomic alterations. Traditional secondary workflows frequently ignore alternative transcripts by averaging or discarding redundant microarray probes, which dilutes essential biological signals.
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To advance our foundational 2018 bioinformatic framework by performing a high-resolution transcriptomic analysis of four core molecular hallmarks in psoriasis - canonical TNF-α signaling, the IL-6 transduction core, the S100 calcium-binding family, and the EGFL8 pathway grid- using a refined probe-selection protocol.
Public transcriptomic data from the NCBI GEO series GSE13355 (GPL570 platform), comprising paired lesional (PP) and non-lesional (PN) skin biopsies alongside healthy controls (NN), were analyzed using R-limma. Methodologically, cross-hybridizing _x_at probes were excluded, while unique _at and shared _s_at probes were retained to capture splice variants. Multiple probes targeting the same gene symbol were collapsed by selecting the single most informative probe based on the highest absolute t-statistic.
The S100 family displayed the highest magnitude of differential expression, led by the massive upregulation of alarmins S100A12 (logFC = 5.8263) and S100A9 (logFC = 5.8228). Within the TNF-α and IL-6 panels, NFKB1 (logFC = 0.5161) and STAT3 (logFC = 1.0926) were identified as dominant transcriptional nodes. Retaining _s_at probes proved essential to capture primary reactive signals for STAT3 and IKBKG. Furthermore, the EGFL8 grid revealed significant cell cycle acceleration via MAP2K1 and CDK1 induction.
By refining microarray probe curation, this study successfully improves the data consistency of our original model, providing a precise, systems-level resolution of the molecular hallmarks sustaining psoriatic lesions.
This is a preprint: it has not been peer reviewed yet, and its findings may change.
Published in Research Square (preprint). The abstract is shown as published and remains the work of its authors; read the full article at the source.
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