Human Gene Set: THEILGAARD_NEUTROPHIL_AT_SKIN_WOUND_DN


Standard name THEILGAARD_NEUTROPHIL_AT_SKIN_WOUND_DN
Systematic name M11234
Brief description Genes down-regulated in polymorphonuclear neutrophilic granulocytes (PMNs) attracted to skin wounds.
Full description or abstract To investigate the cellular fate and function of polymorphonuclear neutrophilic granulocytes (PMNs) attracted to skin wounds, we used a human skin-wounding model and microarray technology to define differentially expressed genes in PMNs from peripheral blood, and PMNs that had transmigrated to skin lesions. After migration to skin lesions, PMNs demonstrated a significant transcriptional response including genes from several different functional categories. The up-regulation of anti-apoptotic genes concomitant with the down-regulation of proapoptotic genes suggested a transient anti-apoptotic priming of PMNs. Among the up-regulated genes were cytokines and chemokines critical for chemotaxis of macrophages, T cells, and PMNs, and for the modulation of their inflammatory responses. PMNs in skin lesions down-regulated receptors mediating chemotaxis and anti-microbial activity, but up-regulated other receptors involved in inflammatory responses. These findings indicate a change of responsiveness to chemotactic and immunoregulatory mediators once PMNs have migrated to skin lesions and have been activated. Other effects of the up-regulated cytokines/chemokines/enzymes were critical for wound healing. These included the breakdown of fibrin clots and degradation of extracellular matrix, the promotion of angiogenesis, the migration and proliferation of keratinocytes and fibroblasts, the adhesion of keratinocytes to the dermal layer, and finally, the induction of anti-microbial gene expression in keratinocytes. Notably, the up-regulation of genes, which activate lysosomal proteases, indicate a priming of skin lesion-PMNs for degradation of phagocytosed material. These findings demonstrate that migration of PMNs to skin lesions induces a transcriptional activation program, which regulates cellular fate and function, and promotes wound healing.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 15187151   Authors: Theilgaard-Mönch K,Knudsen S,Follin P,Borregaard N
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Source species Homo sapiens
Contributed by Kevin Vogelsang (MSigDB Team)
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identifier namespace		 AFFY_HG_U95
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Version history 3.0: Renamed from KNUDSEN_PMNS_DN

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