Cyclooxygenases in the skin: pharmacological and toxicological implications

Lee, Juliette L; Mukhtar, Hasan; Bickers, David R.; Kopelovich, Levy; Athar, Mohammad

doi:10.1016/s0041-008x(03)00301-6

Cited by 165 publications

(147 citation statements)

References 103 publications

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“…COX-1 and -2 isoenzymes have to be coupled with various PG synthases to allow the final formation of different PG molecules (27). mRNA for membrane-associated PGE synthase 1, cytosolic PGE synthase, and hematopoietic PGD synthase was abundantly expressed, whereas expression of prostacyclin synthase and thromboxane synthase was present but weak in late wound tissue (Fig.…”

Section: Resultsmentioning

confidence: 99%

Wound Inflammation in Diabeticob/obMice

et al. 2005

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This study focused on the regulation of prostaglandin (PG) production in diabetes-impaired wound tissue. Cyclooxygenase (COX)-1 and -2 expression and activity were severely dysregulated in chronic wounds of diabetic ob/ob mice. Those wounds were characterized by a reduced expression of COX-1 and the presence of strongly elevated levels of COX-2 when compared with conditions observed in healthy animals. Resolution of the diabetic and impaired wound-healing phenotype by systemic administration of leptin into ob/ob mice increased COX-1 expression in wound margin keratinocytes and decreased COX-2 expression in inner wound areas to levels found in wild-type animals. Notably, improved wound healing was characterized by a marked increase in PGE 2 /PGD 2 biosynthesis that colocalized with induced COX-1 in new tissue at the margin of the wound. COX-2 expression did not significantly contribute to PGE 2 /PGD 2 production in impaired wound tissue. Accordingly, only late wound tissue from SC-560 -treated (selective COX-1 inhibitor) but not celecoxibtreated (selective COX-2 inhibitor) ob/ob mice exhibited a severe loss in PGE 2 , PGD 2 , and prostacyclin at the wound site, and this change was associated with reduced keratinocyte numbers in the neo-epithelia. These data constitute strong evidence that a dysregulation of COX-1-coupled prostaglandin contributes to diabetes-impaired wound healing. Diabetes 54: 1543-1551, 2005

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Section: Resultsmentioning

confidence: 99%

Wound Inflammation in Diabeticob/obMice

et al. 2005

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“…Conversely, an actual protective effect of acetaminophen is plausible, eg, through COX-3 inhibition or activation by tyrosinase to cytotoxic metabolites in melanocytes. 39,40 The clinical data on this association, however, are limited and conflicting. 4,13,35,41 When interpreting these discrepancies, our lack of information on over-the-counter acetaminophen should be taken into account.…”

Section: Discussionmentioning

confidence: 99%

Nonsteroidal anti‐inflammatory drugs and the risk of skin cancer

Johannesdottir

Chang

Mehnert

et al. 2012

Cancer

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BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) may prevent the development of cancer by inhibiting cyclooxygenase (COX) enzymes, which are involved in carcinogenesis. Therefore, the authors of this report examined the association between NSAID use and the risk of squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and malignant melanoma (MM). METHODS: From 1991 through 2009, all incident cases of SCC (n ¼ 1974), BCC (n ¼ 13,316), and MM (n ¼ 3242) in northern Denmark were identified. Approximately 10 population controls (n ¼ 178,655) were matched to each case by age, gender, and county of residence. The use of aspirin, other nonselective NSAIDs, or selective COX-2 inhibitors was ascertained through a prescription database. Conditional logistic regression analyses adjusted for potential confounders were used to compute odds ratios as estimates of incidence rate ratios (IRRs). RESULTS: For NSAIDs overall, ever use (>2 prescriptions) compared with nonuse ( 2 prescriptions) was associated with a decreased risk of SCC (IRR, 0.85; 95% confidence interval [CI], 0.76-0.94) and MM (IRR, 0.87; 95% CI, 0.80-0.95), especially for long-term use (!7 years) and high-intensity use (>25% prescription coverage during the total duration of use). NSAID use was not associated with a reduced risk of BCC overall (IRR, 0.97; 95% CI, 0.93-1.01), but the risk of BCC at sites other than the head and neck was reduced in association with long-term use (IRR, 0.85; 95% CI,) and high-intensity use (IRR, 0.79; 95% CI, 0.69-0.91). All estimates of reduced risk were driven primarily by the use of nonselective NSAIDs and older COX-2 inhibitors (diclofenac, etodolac, and meloxicam). CONCLUSIONS: The current results indicated that NSAID use may decrease the risk of SCC and MM.

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“…Inflammatory mediators are produced and operate in a network with different roles -pro inflammatory and anti-inflammatory, -pro fibrotic and -anti fibrotic, thus there could be -inter regulation [35][36][37][38][39][40][41]. Our ongoing work investigate the regulation of wound TGF Beta-1 by other inflammatory mediators mainly COX and iNOS.…”

Section: Interrelation Between Inflammatory Mediators In Wound Healinmentioning

confidence: 99%

Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

El-Aleem¹,

Jude²

2017

J Cytol Histol

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Background: Wound healing is a highly ordered dynamic process associated with inflammation at early stages and with permanent scarring at late stages. Scars could be disfiguring and could advance to be hypertrophic or keloid scars, this would have a strong physical and psychological impact on the patients afterward. The role of inflammatory mediators which could be pro-or anti-inflammatory, pro-or -anti fibrotic was the focus of wound healing research for decades and the balance between them is the key factor determining the outcome of healing.

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Cyclooxygenases in the skin: pharmacological and toxicological implications

Cited by 165 publications

References 103 publications

Wound Inflammation in Diabeticob/obMice

Wound Inflammation in Diabeticob/obMice

Nonsteroidal anti‐inflammatory drugs and the risk of skin cancer

Inhibition of Wound TGF Beta-1 by Celecoxib: A Possible Therapeutic Route for Scar Free Wound

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