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Inhibition of cyclooxygenase‐1 and ‐2 activity in keratinocytes inhibits PGE2 formation and impairs vascular endothelial growth factor release and neovascularisation in skin wounds
This study investigated the role of Cox activity in the regulation of vascular endothelial growth factor (VEGF) expression in keratinocytes and the formation of new blood vessels in acute wounds in mice. To this end, human HaCaT keratinocytes were stimulated with epidermal growth factor (EGF). EGF increased Cox‐1 mRNA in the presence of the constitutively expressed Cox‐1 protein in keratinocytes. EGF coinduced Cox‐2 and VEGF165 mRNA and protein expression and an accumulation of prostaglandin E2 (PGE2) in cell culture supernatants. Inhibition of Cox isozyme activity by Cox‐1 and ‐2 siRNA or ibuprofen reduced PGE2 ...
Source: International Wound Journal - December 17, 2015 Category: Surgery Authors: Itamar Goren, Seo‐Youn Lee, Damian Maucher, Rolf Nüsing, Thomas Schlich, Josef Pfeilschifter, Stefan Frank Tags: ORIGINAL ARTICLE Source Type: research

Inhibition of cyclooxygenase ‐1 and ‐2 activity in keratinocytes inhibits PGE2 formation and impairs vascular endothelial growth factor release and neovascularisation in skin wounds
This study investigated the role of Cox activity in the regulation of vascular endothelial growth factor (VEGF) expression in keratinocytes and the formation of new blood vessels in acute wounds in mice. To this end, human HaCaT keratinocytes were stimulated with epidermal growth factor (EGF). EGF increased Cox‐1 mRNA in the presence of the constitutively expressed Cox‐1 protein in keratinocytes. EGF coinduced Cox‐2 and VEGF165 mRNA and protein expression and an accumulation of prostaglandin E2 (PGE2) in cell culture supernatants. Inhibition of Cox isozyme activity by Cox‐1 and ‐2 siRNA or ibuprofen reduced PGE2 ...
Source: International Wound Journal - December 16, 2015 Category: Surgery Authors: Itamar Goren, Seo ‐Youn Lee, Damian Maucher, Rolf Nüsing, Thomas Schlich, Josef Pfeilschifter, Stefan Frank Tags: ORIGINAL ARTICLE Source Type: research