Ultraviolet B (UVB)-Induced COX-2 Expression in Murine Skin: An Immunohistochemical Study

Athar, Mohammad; An, Kathy P.; Morel, Kimberly D.; Kim, Arianna L.; Aszterbaum, Michelle; Longley, Jack; Epstein, Ervin; Bickers, David R.

doi:10.1006/bbrc.2000.4201

Cited by 120 publications

(112 citation statements)

References 36 publications

(34 reference statements)

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“…These data are consistent with earlier reports showing that UVB effectively induces COX-2 in mouse and human keratinocytes (Isoherranen et al, 1999;Black et al, 2008). Our data also demonstrate that differentiated cells are more sensitive to UVB-induced upregulation of COX-2 mRNA and protein, a finding consistent with previous studies showing that UVB-induced COX-2 expression in mouse skin occurs primarily in the suprabasal, differentiated keratinocytes (Athar et al, 2001). At the present time, the mechanisms underlying the increased sensitivity of differentiated cells to UVB are not known although it should be noted that abnormal differentiation occurs in mouse epidermis following overexpression of COX-2 (Neufang et al, 2001).…”

Section: Discussionsupporting

confidence: 94%

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: Discussionsupporting

confidence: 94%

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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“…COX-2 over-expression has also been determined in mice models of skin abnormalities, such as hyperplasia of the skin, benign papillomas and SCC -resulting from UV chronic irradiation-. In these animal models COX-2 expression was also found increased in all cases, in accordance with the results obtained in human biopsy samples abovementioned Athar et al, 2001). …”

Section: Epidemiological Datasupporting

confidence: 90%

Cyclooxygenase-2 Overexpression in Non-Melanoma Skin Cancer: Molecular Pathways Involved as Targets for Prevention and Treatment

Maglio¹,

Paz²,

Maiten³

et al. 2011

Skin Cancers - Risk Factors, Prevention and Therapy

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“…Infl ammation and DNA damage occur with UVB irradiation which lead to COX-2 and PCNA expressions [30,31] . PCNA expression is a marker of DNA repair and indirectly an indicator of UVB-induced damage [14] .…”

Section: Discussionmentioning

confidence: 99%

Topical delivery of silymarin constituents via the skin route

et al. 2009

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Aim: Silibinin (SB), silydianin (SD), and silychristin (SC) are components of silymarin. These compounds can be used to protect the skin from oxidative stress induced by ultraviolet (UV) irradiation and treat it. To this end, the absorption of silymarin constituents via the skin was examined in the present report. Methods: Transport of SB, SD, and SC under the same thermodynamic activity through and into the skin and the effects of pH were studied in vitro using a Franz diffusion assembly. Results: The lipophilicity increased in the order of SC

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Ultraviolet B (UVB)-Induced COX-2 Expression in Murine Skin: An Immunohistochemical Study

Cited by 120 publications

References 36 publications

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

UVB light upregulates prostaglandin synthases and prostaglandin receptors in mouse keratinocytes

Cyclooxygenase-2 Overexpression in Non-Melanoma Skin Cancer: Molecular Pathways Involved as Targets for Prevention and Treatment

Topical delivery of silymarin constituents via the skin route

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