Okan Gökhan, Yıldız Zeynep, Gökdemir Gonca, Yorulmaz Eda, Vural Pervin, Doğru-Abbasoğlu Semra, Uysal Müjdat
Medical Park Bahçelievler Hospital, Dermatology Clinic, Istanbul, Turkey.
Department of Biochemistry, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey.
Indian J Dermatol. 2015 Mar-Apr;60(2):211. doi: 10.4103/0019-5154.152561.
The etiopathogenesis of psoriasis has not been clearly elucidated although the role of chronic inflammation, imbalance between pro- and anti-inflammatory cytokines, and many immunological events have been established. Endothelin 1 (EDN1) and endothelin receptor type-A (EDNRA) are implicated in the inflammatory process. The relationships between EDN1 and EDNRA polymorphisms with several diseases have been found.
This study examined the possible association of EDN1 (G5665T and T-1370G) and EDNRA (G-231A and G + 70C) single nucleotide polymorphisms (SNPs) with the occurence of psoriasis, and evaluated the relationship between genotypes and clinical/laboratory manifestation of psoriasis.
We analyzed genotype and allele distributions of the above-mentioned polymorphisms in 151 patients with psoriasis and 152 healthy controls by real-time PCR combined with melting curve analysis.
We did not find significant differences in the genotype and allele distributions of EDN1 T-1370G, EDNRA G-231A, and EDNRA G+70C polymorphisms between patients with psoriasis and healthy controls. Psoriasis area and severity index (PASI) score of EDNRA -231 polymorphic A allele carrying subjects (AA and AA + AG) was higher than that of wild homozygotes (P = 0.044 and P = 0.027, respectively). In addition, EDN1 levels in EDNRA+70 polymorphic C allele carriers (CC + CG) were elevated when compared with GG genotype; however, the difference was at borderline significance (P = 0.05).
Although there were no associations between studied polymorphisms and psoriasis susceptibility, the PASI score and EDN1 levels seem to be affected by EDNRA G-231A and G + 70C polymorphisms.
尽管慢性炎症、促炎细胞因子与抗炎细胞因子之间的失衡以及许多免疫事件在银屑病发病机制中的作用已得到确认,但银屑病的确切发病机制尚未完全阐明。内皮素1(EDN1)和A型内皮素受体(EDNRA)参与了炎症过程。研究发现EDN1和EDNRA基因多态性与多种疾病之间存在关联。
本研究旨在探讨EDN1基因(G5665T和T-1370G)和EDNRA基因(G-231A和G+70C)单核苷酸多态性(SNP)与银屑病发病的可能关联,并评估这些基因型与银屑病临床/实验室表现之间的关系。
采用实时荧光定量PCR结合熔解曲线分析技术,对151例银屑病患者和152例健康对照者上述基因多态性的基因型和等位基因分布进行分析。
银屑病患者与健康对照者在EDN1基因T-1370G、EDNRA基因G-231A和EDNRA基因G+70C多态性的基因型和等位基因分布上未发现显著差异。携带EDNRA基因-231多态性A等位基因的受试者(AA和AA+AG)的银屑病面积和严重程度指数(PASI)评分高于野生纯合子(P值分别为0.044和0.027)。此外,与GG基因型相比,携带EDNRA基因+70多态性C等位基因的受试者(CC+CG)的EDN1水平升高,但差异接近显著性(P=0.05)。
尽管所研究的基因多态性与银屑病易感性之间无关联,但PASI评分和EDN1水平似乎受EDNRA基因G-231A和G+70C多态性的影响。