CONTRIBUTION OF UVB AND UVA TO UV- DEPENDENT STIMULATION OF CYCLOOXYGENASE-2 EXPRESSION IN ARTIFICIAL EPIDERMIS.
Both UVB (280–320 nm) and UVA (320–400 nm) radiation lead to an enhanced expression of cyclooxygenase-2 (COX-2) in epidermal cells in various in-vitro and in-vivo models. It is demonstrated here that the expression of COX-2 is induced in artificial human epidermis exposed to simulated solar light (>290 nm). Employing filters eliminating specified regions from the simulated solar spectrum, the UVB and UVA-2 (320–350 nm) regions are shown to fully account for induction of COX-2 mRNA and protein as well as the enhanced production of prostaglandin E2 after irradiation. At the protein level, approximately 70% of the total induction by solar light is due to light in the UVA-2 region. UVA-1 (350–400 nm), visible light and IR radiation are practically ineffective. COX-2 induction by simulated solar light is attenuated in the presence of inhibitors of p38MAPK or of c-Jun-N-terminal kinases (JNK), whereas COX-2 induction by UVA is blocked only by inhibition of JNK. UV-induced COX-2 expression is not affected by inhibition of the MEK 1,2/ERK 1,2 pathway.
COX-1, COX-2, Cyclooxygenases (COX), Cytokines, EPI-100-MM, In vitro, In vivo, Jun-N-terminal kinase (JNK), MTT, MTT assay, Messenger RNA (mRNA), Mitogen-activated protein kinase (MAPK), Prostaglandin E2, Radiation, Reverse transcription-polymerase chain reaction (RT-PCR), Solar light (SSL), Triton X-100, UVA, UVA-2, UVB, UVB region
EPI-100-MM, UV (SS), UVA
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