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银屑病皮肤及细胞因子刺激的培养角质形成细胞中诱导型一氧化氮合酶表达增加。

Increased expression of inducible nitric oxide synthase in psoriatic skin and cytokine-stimulated cultured keratinocytes.

作者信息

Sirsjö A, Karlsson M, Gidlöf A, Rollman O, Törmä H

机构信息

Clinical Research Centre, University Hospital, Linköping, Sweden.

出版信息

Br J Dermatol. 1996 Apr;134(4):643-8. doi: 10.1111/j.1365-2133.1996.tb06963.x.

DOI:10.1111/j.1365-2133.1996.tb06963.x
PMID:8733364
Abstract

Since nitric oxide (NO) has been implicated in the pathogenesis of various hyperproliferative and inflammatory diseases, the mRNA expression of constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) were investigated in psoriatic skin by reverse transcriptase coupled to the polymerase chain reaction (PCR). The study showed that the mRNA expression of brain nitric oxide synthase (bNOS), one of two isoforms of cNOS, was weak in both psoriatic plaques lesions and uninvolved skin, while mRNA transcripts for the second isoform, endothelial nitric oxide synthase (eNOS), were not detectable using the present method. In contrast, the mRNA expression of iNOS was markedly increased in lesional skin as compared to uninvolved skin. Cultured human keratinocytes exposed to a combination of interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) for 4 h, showed strong gene expression of iNOS, while in 24 h, the expression had returned to baseline expression. In summary, the study demonstrates that mRNA for the inducible form of NOS is over-expressed in psoriatic lesions. The cause of this may be the local presence of inflammatory cytokines. These findings imply that iNOS may play an important part in local regulation of NO synthesis in psoriasis and other inflammatory dermatoses.

摘要

由于一氧化氮(NO)与多种增殖性和炎性疾病的发病机制有关,因此通过逆转录聚合酶链反应(PCR)研究了银屑病皮肤中组成型一氧化氮合酶(cNOS)和诱导型一氧化氮合酶(iNOS)的mRNA表达。研究表明,cNOS的两种同工型之一——脑一氧化氮合酶(bNOS)的mRNA表达在银屑病斑块病变和非病变皮肤中均较弱,而使用本方法未检测到第二种同工型——内皮型一氧化氮合酶(eNOS)的mRNA转录本。相反,与非病变皮肤相比,iNOS的mRNA表达在病变皮肤中明显增加。培养的人角质形成细胞暴露于白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的组合中4小时,显示出iNOS的强基因表达,而在24小时时,表达已恢复到基线表达。总之,该研究表明,诱导型NOS的mRNA在银屑病病变中过度表达。其原因可能是炎性细胞因子的局部存在。这些发现表明,iNOS可能在银屑病和其他炎性皮肤病中NO合成的局部调节中起重要作用。

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