Ultraviolet B Irradiation Induces Changes in the Distribution and Release of Arachidonic Acid, Dihomo-γ-linolenic Acid, and Eicosapentacnoic Acid in Human Keratinocytes in Culture

Punnonen, Kari; Puustinen, Tapio; Jansén, Christer T.

doi:10.1111/1523-1747.ep12470217

Cited by 43 publications

(21 citation statements)

References 10 publications

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“…The initial step of prostanoid biosynthesis is mobilization of arachidonic acid from phospholipid membranes through the action of phospholipases (Funk, 2001). Previous studies reported that UVB stimulates arachidonic acid release from membrane phospholipids (DeLeo et al, 1985;Punnonen et al, 1987), as well as cPLA 2 synthesis and activity in skin (KangRotondo et al, 1993;Gresham et al, 1996). In contrast, we found no major changes in cPLA 2 mRNA expression in undifferentiated or differentiated mouse keratinocytes following UVB light treatment.…”

Section: Discussioncontrasting

confidence: 62%

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

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Gray

Shakarjian

et al. 2008

Toxicology and Applied Pharmacology

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Prostaglandins belong to a class of cyclic lipid-derived mediators synthesized from arachidonic acid via COX-1, COX-2 and various prostaglandin synthases. Members of this family include prostaglandins such as PGE 2 , PGF 2α , PGD 2 and PGI 2 (prostacyclin) as well as thromboxane. In the present studies we analyzed the effects of UVB on prostaglandin production and prostaglandin synthase expression in primary cultures of undifferentiated and calcium-differentiated mouse keratinocytes. Both cell types were found to constitutively synthesize PGE 2 , PGD 2 and the PGD 2 metabolite PGJ 2 . Twenty-four hr after treatment with UVB (25 mJ/cm 2 ), production of PGE 2 and PGJ 2 increased, while PGD 2 production decreased. This was associated with increased expression of COX-2 mRNA and protein. UVB (2.5 -25 mJ/cm 2 ) also caused marked increases in mRNA expression for the prostanoid synthases PGDS, mPGES-1, mPGES-2, PGFS and PGIS, as well as expression of receptors for PGE 2 (EP1 and EP2), PGD 2 (DP and CRTH2) and prostacyclin (IP). UVB was more effective in inducing COX-2 and DP in differentiated cells and EP1 and IP in undifferentiated cells. UVB readily activated keratinocyte PI-3-kinase (PI3K)/Akt, JNK and p38 MAP signaling pathways which are known to regulate COX-2 expression. While inhibition of PI3K suppressed UVB-induced mPGES-1 and CRTH2 expression, JNK inhibition suppressed mPGES-1, PGIS, EP2 and CRTH2, and p38 kinase inhibition only suppressed EP1 and EP2. These data indicate that UVB modulates expression of prostaglandin synthases and receptors by distinct mechanisms. Moreover, both the capacity of keratinocytes to generate prostaglandins and their ability to respond to these lipid mediators are stimulated by exposure to UVB.

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Section: Discussioncontrasting

confidence: 62%

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

Black

Gray

Shakarjian

et al. 2008

Toxicology and Applied Pharmacology

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“…Because melatonin is not metabolized in the human skin [15], and a light absorptive effect of melatonin has been excluded in the present study, there must be another mechanism of inflammatory inhibition induced by melatonin. There are two possible ways of action: the radical scavenging mechanism of quenching hydroxyl radicals by melatonin or the modification of arachidonic metabolism with reduc- tion of prostaglandins and leukotrienes or both in combination [3,11,16]. A former study with the topical application of melatonin to prevent UV erythema showed a suppressive effect even when melatonin was given immediately after irradiation [12].…”

Section: Discussionmentioning

confidence: 99%

“…Clinical symptoms like erythema, heat, edema, pain and pruritus are caused by the formation of proinflammatory mediators: cytokines, adhesion molecules, vasoactive peptides, arachidonic acid and especially leukotrienes (LTB 4 ) and prostaglandins (PGE 2 and PGD 2 ) as proinflammatory metabolites of arachidonic acid [1][2][3]. There is now increasing evidence that free radicals may be involved in acute sunburn reactions, probably causing damage by peroxidation of important intra-and extracellular biochemical structures, e.g.…”

Section: Introductionmentioning

confidence: 99%

Suppression of UV-Induced Erythema by Topical Treatment with Melatonin

Fischer

Bangha²,

Elsner³

et al. 1999

Neurosignals

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The UV-suppressive effect of topical melatonin was assessed at different application time points in a double-blind randomized clinical trial. The lower back of 20 healthy volunteers was treated with 0.6 mg/cm² melatonin or vehicle either 15 min before or 1, 30 or 240 min after UV irradiation. The erythema was evaluated visually and measured by chromametry 24 h after irradiation. UV-absorbing effects of melatonin were measured at a concentration of 8 µg/ml with a spectrophotometer. Melatonin absorbs UV light at a wavelength of 225–275 nm which is clearly below the wavelength of UVA and UVB (290–390 nm). The visual score showed that application of melatonin 15 min before irradiation significantly suppressed erythema compared to treatment with vehicle alone (p < 0.001). Similar results were found by chromametry (p < 0.001). Treatment after irradiation showed no UV suppression. The erythema suppressive effect of melatonin might be explained by the radical-scavenging mechanism of quenching meanly hydroxyl radicals (·OH) which are known to be most present in sunburn reaction of the skin. The protective effect of the pre-irradiation treatment might be explained by penetration into the skin within 15 min and the presence in a local concentration at the irradiation time point.

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“…Furthermore, it has heen suggested that the synthesis or secretion of several soluhle mediators and cytokines, including interleukin-l [22,23], eicosanoids [24], cis-urocanic acid [25,26], and tumor necrosis factor-a [25], is responsihle for immunosuppression after UVB radiation.…”

mentioning

confidence: 99%

Ultraviolet B-Induced Local Immunosuppression of Contact Hypersensitivity Is Modulated by Ultraviolet Irradiation and Hapten Application

Miyauchi

Horio

1995

Journal of Investigative Dermatology

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The induction of contact hypersensitivity is suppressed when hapten is applied topically to an area irradiated by ultraviolet B (UVB). There is no standardized procedure to induce this local immunosuppression by UVB. We investigated the effects of the following factors on induction of dinitrofluorobenzene contact hypersensitivity in mice. UVB dose, divided UVB exposure, timing of sensitization after irradiation, hapten concentration, hapten volume (application area), sex, age, and simultaneous sensitization on UV-exposed and nonexposed skin. The suppression was enhanced by increasing the UVB dose. When 100 mJ/cm2 of UVB was irradiated, divided daily exposure (25 mJ x 4 d) was more suppressive than single exposure (100 mJ x 1 d). Sensitization 2 d after irradiation (100 mJ/cm2) induced suppression most effectively. When 25 microliters of dinitrofluorobenzene solution was applied to exposed skin, higher concentrations induced lower suppression. When the total dose of hapten was kept constant (92 micrograms), the application of lower concentrations to large areas (0.25%, 25 microliters) caused stronger suppression than higher concentrations (1%, 6.25 microliters) to small areas. Simultaneous sensitization on UV-exposed and nonexposed skin revealed less suppression than sensitization only on exposed skin. The suppression of contact hypersensitivity was significantly greater in young than in old mice. These results provide details that may be useful in designing studies involving immunosuppression by UVB radiation.

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Ultraviolet B Irradiation Induces Changes in the Distribution and Release of Arachidonic Acid, Dihomo-γ-linolenic Acid, and Eicosapentacnoic Acid in Human Keratinocytes in Culture

Cited by 43 publications

References 10 publications

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

Suppression of UV-Induced Erythema by Topical Treatment with Melatonin

Ultraviolet B-Induced Local Immunosuppression of Contact Hypersensitivity Is Modulated by Ultraviolet Irradiation and Hapten Application

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