Kim Nan-Hyung, Choi Soo-Hyun, Lee Tae Ryong, Lee Chang-Hoon, Lee Ai-Young
Department of Dermatology, Dongguk University Ilsan Hospital, 814 Siksa-dong, Ilsandong-gu, Goyang-si, Gyeonggi-do 410-773, Korea.
Acta Derm Venereol. 2016 Jun 15;96(5):635-40. doi: 10.2340/00015555-2315.
Basement membrane (BM) disruption and dermal changes (elastosis, collagenolysis, vascular ectasia) have been reported in melasma. Although ultraviolet (UV) irradiation can induce these changes, UV is not always necessary for melasma development. Cadherin 11 (CDH11), which is upregulated in some melasma patients, has previously been shown to stimulate melanogenesis. Because CDH11 action requires cell-cell adhesion between fibroblasts and melanocytes, BM disruption in vivo should facilitate this. The aim of this study was to examine whether CDH11 overexpression leads to BM disruption and dermal changes, independent of UV irradiation. Immunohistochemistry/immunofluorescence, real-time PCR, Western blotting, and zymography suggested that BM disruption/dermal changes and related factors were present in the hyperpigmented skin of CDH11-upregulated melasma patients and in CDH11-overexpressing fibroblasts/keratinocytes. The opposite was seen in CDH11-knockdown cells. UV irradiation of the cultured cells did not increase CDH11 expression. Collectively, these data demonstrate that CDH11 overexpression could induce BM disruption and dermal changes in melasma, regardless of UV exposure.
黄褐斑患者已出现基底膜(BM)破坏和皮肤变化(弹性组织变性、胶原溶解、血管扩张)。尽管紫外线(UV)照射可诱发这些变化,但紫外线并非黄褐斑发病的必要条件。钙黏蛋白11(CDH11)在部分黄褐斑患者中表达上调,此前研究表明其可刺激黑素生成。由于CDH11发挥作用需要成纤维细胞和黑素细胞之间的细胞间黏附,因此体内BM破坏应有助于这一过程。本研究旨在探讨CDH11过表达是否会导致BM破坏和皮肤变化,且不受紫外线照射影响。免疫组织化学/免疫荧光、实时聚合酶链反应、蛋白质免疫印迹和酶谱分析表明,BM破坏/皮肤变化及相关因子存在于CDH11上调的黄褐斑患者色素沉着皮肤以及过表达CDH11的成纤维细胞/角质形成细胞中。而在CDH11基因敲低的细胞中则出现相反情况。对培养细胞进行紫外线照射并未增加CDH11表达。总体而言,这些数据表明,无论紫外线暴露情况如何,CDH11过表达均可诱发黄褐斑中的BM破坏和皮肤变化。