Ultraviolet Radiation Stimulates the Release of Arachidonic Acid From Mammalian Cells in Culture*

Leo, Vincent A. De; Hanson, Deborah K.; Weinstein, I. Bernard; Harber, Leonard C.

doi:10.1111/j.1751-1097.1985.tb03447.x

Cited by 49 publications

(8 citation statements)

References 17 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: 64%

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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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: 64%

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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“…It is known that normal human melanocytes respond directly to UVR (Friedman and Gilchrest, 1987;Halaban et al, 1988;Libow et al, 1988;Quevedo et al, 1969). In addition, there is evidence that UVR acts through cell-membrane-mediated events in human and murine cells in culture, with stimulation of choline phospholipid and arachidonic acid metabolism (DeLeo et al , 1985). Finally, both short-wave (290-320 nm) and long-wave (320-400 nm) UVR result in melanogenesis in human skin (Pathak et al, 1962).…”

Section: Resultsmentioning

confidence: 99%

Action of Light on Frog Pigment Cells in Culture

Daniolos¹,

Lerner²,

Lerner³

1990

Pigment Cell Research

154

121

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Solar radiation induces numerous biologic effects in skin but the mechanism underlying these responses is poorly understood. To study the etiology of these phenomena, we investigated the effect of light on cultured Xenopus laevis melanophores. Visible light stimulated a marked increase in intracellular cAMP levels within the first minute of irradiation. This light-induced elevation in cAMP was blocked by melatonin and was not seen in fibroblasts irradiated in a similar manner. These data show that the photoresponse of pigment cells from amphibian skin can be mediated by a cAMP-dependent mechanisms and suggest that a unique member of the rhodopsin family is involved in this process.

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“…Chronic UVB–mediated inflammation causes the constitutive induction of the COX‐2 enzyme in the skin [10,13,14], resulting in increased prostaglandin levels, inflammatory cell infiltration and activation, and further oxidant production. Prostaglandin production in the skin is induced following UV irradiation as a result of both an increased release of arachidonic acid by phospholipases and by the induction of COX‐2 message and protein levels [9,11,15–21]. The resulting prostaglandin E 2 (PGE 2 ) acts as a promoter in the carcinogenesis process [22] by contributing to the uncontrolled proliferation of damaged cells that ultimately form tumors in the skin.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of cutaneous ultraviolet light B–mediated inflammation and tumor formation with topical celecoxib treatment

Wilgus

Koki²,

Zweifel³

et al. 2003

Molecular Carcinogenesis

142

148

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Inflammation, which includes the release of growth factors, proinflammatory cytokines and prostaglandins, the infiltration and activation of inflammatory cells, and the induction of oxidative DNA damage, is known to play a role in cancer development. The combination of damage to the skin resulting from chronic ultraviolet light B (UVB) exposure itself and the inflammatory response it induces is a major source of skin cancer development. Cyclooxygenase-2 (COX-2), an inflammatory enzyme responsible for the production of prostaglandins, is now implicated in the development of epithelial cancers, including squamous cell carcinoma in the skin. Previous work conducted in our laboratory has shown that topical treatment with celecoxib following UVB irradiation inhibits several parameters of acute inflammation, including vascular permeability, the infiltration and activation of neutrophils, and the production of prostaglandin E(2) (PGE(2)). The present studies expanded these observations, demonstrating the ability of topical celecoxib to inhibit acute oxidative damage. In addition, long-term studies illustrate the effectiveness of topical treatment with this drug in reducing chronic inflammation and UVB-induced papilloma/carcinoma formation. This data provides compelling evidence to explore the clinical efficacy of topically applied COX-2 inhibitors for the prevention of human skin cancers.

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Ultraviolet Radiation Stimulates the Release of Arachidonic Acid From Mammalian Cells in Culture*

Cited by 49 publications

References 17 publications

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

Action of Light on Frog Pigment Cells in Culture

Inhibition of cutaneous ultraviolet light B–mediated inflammation and tumor formation with topical celecoxib treatment

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