Arachidonic Acid-Derived Bioactive Lipids: Their Role and the Role for Their Inhibitors in Dermatology

Smith, Kathleen J.; Skelton, Henry G.

doi:10.1177/120347540200600309

Cited by 5 publications

(3 citation statements)

References 138 publications

(53 reference statements)

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“…Prostaglandins are lipid‐derived mediators that have a wide spectrum of biological activities that is determined by their tissue of origin [1,2]. In the skin they mediate inflammatory reactions, although the sequence of events involved in these responses is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin production by melanocytic cells and the effect of α‐melanocyte stimulating hormone

et al. 2004

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Prostaglandins are potent mediators of the inflammatory response and are also involved in cancer development. In this study, we show that human melanocytes and FM55 melanoma cells express cyclooxygenase-1 and -2 (COX-1 and -2) and thus have the capability to produce prostaglandins. The FM55 cells produced predominantly PGE 2 and PGF 2a , whereas the HaCaT keratinocyte cell line produced mainly PGE 2 . The anti-inflammatory peptide, a-melanocyte stimulating hormone (a-MSH), reduced prostaglandin production in FM55 and HaCaT cells and reversed the effect of the pro-inflammatory cytokine TNF-a in the former. These results indicate that melanocytes produce prostaglandins and that a-MSH, by inhibiting this response, may play an important role in regulating inflammatory responses in the skin.

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Section: Introductionmentioning

confidence: 99%

Prostaglandin production by melanocytic cells and the effect of α‐melanocyte stimulating hormone

et al. 2004

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“…Leukotrienes are proinflammatory lipids implicated in the pathogenesis of inflammation-driven diseases, including asthma, atopic dermatitis, reperfusion injury, immediate hypersensitivity reactions, adaptive immune responses, rheumatoid arthritis, inflammatory bowel disease, and psoriasis (1,2). Leukotriene B4 (LTB4) mediates innate immune responses by modulating leukocyte effector functions and production of chemokines and cytokines that amplify inflammation (3).…”

mentioning

confidence: 99%

“…Metabolic inactivation of leukotriene signaling has been ignored as a proresolving mechanism due to the dearth of knowledge concerning how catabolic pathways are regulated, especially in peripheral tissues afflicted in common inflammatory diseases. The potent chemoattractant LTB4 is inactivated mainly by hydroxylation at the -terminus, catalyzed by cytochromes P450 CYP4F3A and CYP4F2 (CYP gene products) in human neutrophils and liver, respectively (2,6,7). Proresolving actions of CYP4F enzymes are further supported by their increased expression in various organ systems following traumatic brain injury or challenge with proinflammatory mediators (6,8,9).…”

mentioning

confidence: 99%

Inflammation resolved by retinoid X receptor‐mediated inactivation of leukotriene signaling pathways

Kalsotra¹,

Du²,

Wang³

et al. 2007

FASEB j.

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Leukotrienes are implicated in the pathogenesis of diverse, inflammation-driven diseases. Metabolic inactivation of leukotriene signaling is an innate response to resolve inflammation, yet little is known of mechanisms regulating disposition of leukotrienes in peripheral tissues afflicted in common inflammatory diseases. We studied leukotriene hydroxylases (CYP4F gene products) in human skin, a common target of inflammation and adverse drug reactions. Epidermal keratinocytes express at least six CYP4F enzymes; the most highly expressed and highly regulated is CYP4F3A-the main neutrophil leukotriene hydroxylase. Differentiation-specific factors and retinoids are positive CYP4F regulators in vitro, effecting increased leukotriene B4 hydroxylation (inactivation). CYP4F expression is up-regulated in situ in hyperproliferative dermatoses-an innate mechanism to repair and restore epidermal barrier competency-and after retinoid therapy. Enhanced CYP4F-mediated inactivation of leukotriene signaling is a previously unrecognized antiinflammatory property of therapeutic retinoids mediated by preferential interactions between retinoid X receptors and CYP4F promoter elements in epidermal cells.

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Enzymes involved in the biosynthesis of leukotriene B4 and prostaglandin E2 are active in sebaceous glands

et al. 2005

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The expression of enzymes involved in leukotriene and prostaglandin signalling pathways, of interleukins 6 and 8 and of peroxisome proliferator-activated receptors in sebaceous glands of acne-involved facial skin was compared with those of non-involved skin of acne patients and of healthy individuals. Moreover, 5-lipoxygenase and leukotriene A(4) hydrolase were expressed at mRNA and protein levels in vivo and in SZ95 sebocytes in vitro (leukotriene A(4) hydrolase > 5-lipoxygenase), while 15-lipoxygenase-1 was only detected in cultured sebocytes. Cyclooxygenase-1 and cyclooxygenase-2 were also present. Peroxisome proliferator-activated receptors were constitutively expressed. Enhanced 5-lipoxygenase, cyclooxygenase 2 and interleukin 6 expression was detected in acne-involved facial skin. Arachidonic acid stimulated leukotriene B(4) and interleukin 6 release as well as prostaglandin E(2) biosynthesis in SZ95 sebocytes, induced abundant increase in neutral lipids and down-regulated peroxisome proliferator-activated receptor-alpha, but not receptor-gamma1 mRNA levels, which were the predominant peroxisome proliferator-activated receptor isotypes in SZ95 sebocytes. In conclusion, human sebocytes possess the enzyme machinery for functional leukotriene and prostaglandin pathways. A comprehensive link between inflammation and sebaceous lipid synthesis is provided.

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Arachidonic Acid-Derived Bioactive Lipids: Their Role and the Role for Their Inhibitors in Dermatology

Cited by 5 publications

References 138 publications

Prostaglandin production by melanocytic cells and the effect of α‐melanocyte stimulating hormone

Prostaglandin production by melanocytic cells and the effect of α‐melanocyte stimulating hormone

Inflammation resolved by retinoid X receptor‐mediated inactivation of leukotriene signaling pathways

Enzymes involved in the biosynthesis of leukotriene B4 and prostaglandin E2 are active in sebaceous glands

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