Figure 5

Proposed model for regulation of collagen formation in these experiments. 1. Activation of the nuclear factor-κB (NF-κB) signaling pathway by lipopolysaccharide. 2. NO can inhibit the binding of NF-κB family members to target DNA. 3. NF-κB family binding to DNA and transcription of iNOS mRNA. 4. L-NAME inhibits the production of NO from iNOS. 5. NO regulates PGE₂ production divergently through activation of COX isoforms. 6. Indomethacin inhibits COX and reduces PGE₂production. 7. Collagen production and wound healing processes are changed by the activation of different PGE₂ receptors subtypes and second messengers. LPS, lipopolysaccharide; Tlr4, Toll-like receptor 4; Traf6, Tumor necrosis factor receptor-associated factor 6; IκB, Inhibitor of kappa light polypeptide gene enhancer in B-cell; NF-κB, nuclear transcription factor kappaB; iNOS, inducible nitric oxide synthase; L-NAME, NG-nitro-L-arginine methyl ester; NO, nitric oxide; COX, cyclooxygenase; INDO, indomethacin; PKC, protein kinase C; cAMP, cyclic adenosine monophosphate.