Cyclooxygenase-1-coupled prostaglandin biosynthesis constitutes an essential prerequisite for skin repair

被引：65

作者：

Kämpfer, H ^{[1
]}

Bräutigam, L ^{[1
]}

Geisslinger, G ^{[1
]}

Pfeilschifter, J ^{[1
]}

Frank, S ^{[1
]}

机构：

[1] Pharmazentrum Frankfurt, D-60590 Frankfurt, Germany

来源：

JOURNAL OF INVESTIGATIVE DERMATOLOGY | 2003年 / 120卷 / 05期

关键词：

non-steroidal anti-inflammatory agents; dinoprostone; keratinocytes; knock-out mice; prostaglandin endoperoxidase synthase;

D O I：

10.1046/j.1523-1747.2003.12140.x

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

This investigation demonstrated a functional coupling between cyclooxygenase-1 (cox) and prostaglandin E-2/D-2 biosynthesis in murine skin repair. Cyclooxygenase-1 expression decreased transiently after excisional wounding, and this was followed by a marked fall in the rate of prostaglandin E-2/D-2 biosynthesis at the wound site. Expression of cyclooxygenase-1, prostaglandin synthases, and prostaglandin E-2/D-2 production were colocalized in new tissue at the margin of the wound. Although cyclooxygenase-2 expression was strongly induced in granulation tissue on injury, this isoform did not contribute to high prostaglandin E-2/D-2 concentrations in wounds. Accordingly, wound tissue from SC-560-treated mice (selective cyclooxygenase-1 inhibitor) and diclofenac-treated mice (nonselective cyclooxygenase inhibitor), but not celecoxib-treated mice (selective cyclooxygenase-2 inhibitor), and wound tissue from cyclooxygenase-1-deficient animals exhibited a severe loss of prostaglandin E-2/D-2 at the wound site, and this change was associated with an impairment in the normal wound morphology. Topically administered prostaglandin E-2 (dinoprostone) was able to restore normal wound repair to diclofenac-treated mice. In contrast to the presence of an injury-induced cyclooxygenase-2, these data constitute strong evidence that cyclooxygenase-1-coupled prostaglandin E-2/D-2 biosynthesis has a central role in skin repair.

引用

页码：880 / 890

页数：11

共 51 条

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