Psoriatic keratinocytes are resistant to tumor necrosis factor alpha's induction of mRNA for the NMDA‐R2C subunit
Copyright policy )Psoriatic keratinocytes are resistant to tumor necrosis factor alpha's induction of mRNA for the NMDA‐R2C subunit
AbstractPsoriatic individuals demonstrate accelerated healing and the Koebner phenomenon, suggesting that psoriatic proliferation of keratinocytes is not inhibited appropriately after skin injury. Serial analysis of gene expression in TNFα‐exposed keratinocytes shows the greatest alteration in expression of NMDA‐R2C. Expression of the NMDA receptor is altered in diseased skin containing TNFα, and TNFα plays a prominent role in psoriasis. An abnormality in induction of NMDA‐R2C by TNFα in psoriatic keratinocytes may explain their lack of growth inhibition. We compared the capacity of TNFα to induce expression of NMDA‐R2C in normal and psoriatic (involved and uninvolved) keratinocytes in vitro. After 72 h of incubation with TNFα, normal keratinocytes demonstrated a significant induction of NMDA‐R2C mRNA compared with control cultures, whereas psoriatic keratinocytes showed no induction. In an in vitro model of wounding (scratches on monolayers), TNFα inhibited migration/proliferation of keratinocytes only at the edge of NMDA‐R2C expressing wounded monolayers of normal keratinocytes.
- University of California, San Diego United States
Adult, Keratinocytes, Male, Wound Healing, Tumor Necrosis Factor-alpha, Gene Expression Profiling, Cell Differentiation, Receptors, N-Methyl-D-Aspartate, Gene Expression Regulation, Cell Movement, Humans, Psoriasis, Female, RNA, Messenger, Cells, Cultured, Cell Proliferation, Skin
Adult, Keratinocytes, Male, Wound Healing, Tumor Necrosis Factor-alpha, Gene Expression Profiling, Cell Differentiation, Receptors, N-Methyl-D-Aspartate, Gene Expression Regulation, Cell Movement, Humans, Psoriasis, Female, RNA, Messenger, Cells, Cultured, Cell Proliferation, Skin
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