From: Elucidating mechanistic insights into drug action for atopic dermatitis: a systems biology approach
Gene/Pathway | Role in skin pathways | Impact derived from eSkIN |
---|---|---|
TNF pathway | TNF pathway via NF-κB regulates the transcription of inflammatory cytokines, adhesion molecules, MMP9 and SELE. | TNF and its receptors are downregulated after treatment with BM, thus effecting anti-inflammatory effect. |
TLRs | TLRs play important role in inflammation by activating NF-κB, which in turn, activates inflammatory cytokines. | Downregulated after treatment with BM, thus bringing about anti-inflammatory effect. |
IL4 pathway | Involved in T-cell and eosinophil chemotaxis | Downregulated after treatment with BM, thus contributes towards anti-inflammatory effect. |
LOR, FLG, TGM5 and CDSN | Important skin barrier proteins | Upregulated after treatment with BM; contributes towards restoration of skin barrier functions. |
IVL, Keratins, LCEs, desmocollins and desmogleins | Important skin barrier proteins | Downregulated after treatment with BM representing the damage to skin barrier; CD44, AKT1, PKC-δ, HRAS and MAP2K3 involved in pathway leading to transcriptional activation of barrier proteins are also downregulated in BM samples. |
S100 family proteins | Important anti-microbial peptides that help in protecting the skin from infections. | Downregulated after treatment with BM, thus leading to impaired barrier function. |
VEGF | Wound healing and cell migration, vascular permeability, angiogenesis, cell invasion and coagulation | Downregulated after treatment with BM, thus affecting wound healing and other cellular processes through PLC-γ and MAPK cascade. |
H2AFX, RAD51, BRCA2, MCM3, DHFR, HMOX1, GINS1 and PCNA | Genes involved in DNA repair | Downregulated after treatment with BM, thus affecting DNA repair processes. |