Rani Seema, Bhardwaj Supriya, Srivastava Niharika, Sharma Vijay Lakshmi, Parsad Davinder, Kumar Ravinder
Department of Zoology, Panjab University, Chandigarh, 160014, India.
Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Arch Dermatol Res. 2017 Mar;309(2):123-132. doi: 10.1007/s00403-016-1713-0. Epub 2017 Jan 11.
Dermal fibroblasts secrete various growth factors which are important for skin pigmentation. Imbalance in the synchronization of epidermal and dermal cells in the skin can play vital role in the pathogenesis of pigmentary disorder vitiligo. Therefore, our objective was to check the lesional fibroblasts for any abnormality and senescence in non-segmental vitiligo patients (NSV). Skin punch biopsies were taken from NSV patients and healthy controls. Explant culture of fibroblast from lesional dermis, non-lesional dermis, and control was analyzed. The senescence was confirmed by β-galactosidase staining in the cultured fibroblasts. Senescence was checked at mRNA level in lesional dermis, non-lesional dermis of NSV patients by senescence markers p16, p21, and hp1 by quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence study was used for protein analysis. Morphological results showed number of fibroblasts with bigger perinuclear region and vacuoles were more in the lesional fibroblasts. Number of β-galactosidase positive fibroblasts in the lesional skin of NSV patients was higher as compared to the non-lesional and control fibroblasts. Results showed higher relative gene expression of senescence markers p16, p21, and hp1 in the lesional dermis of NSV patients at mRNA level and protein level as compared with control. Senescence in the dermal fibroblasts can decrease the secretion of growth factors and cytokines secreted by fibroblasts which may lead to the melanocyte death and progression of vitiligo. However, further studies on larger number of patients are needed to confirm the role of fibroblasts in the vitiligo pathogenesis.
真皮成纤维细胞分泌多种对皮肤色素沉着至关重要的生长因子。皮肤中表皮细胞和真皮细胞同步失衡在色素性疾病白癜风的发病机制中可能起关键作用。因此,我们的目的是检查非节段性白癜风患者(NSV)的皮损成纤维细胞是否存在任何异常和衰老情况。从NSV患者和健康对照者身上采集皮肤打孔活检组织。对来自皮损真皮、非皮损真皮和对照的成纤维细胞进行外植体培养分析。通过培养的成纤维细胞中的β-半乳糖苷酶染色确认衰老情况。通过衰老标志物p16、p21和hp1,利用定量实时聚合酶链反应(qRT-PCR)在mRNA水平检测NSV患者皮损真皮、非皮损真皮中的衰老情况,并采用免疫荧光研究进行蛋白质分析。形态学结果显示,皮损成纤维细胞中核周区域较大且有液泡的成纤维细胞数量更多。与非皮损和对照成纤维细胞相比,NSV患者皮损皮肤中β-半乳糖苷酶阳性成纤维细胞数量更高。结果显示,与对照相比,NSV患者皮损真皮在mRNA水平和蛋白质水平上衰老标志物p16、p21和hp1的相对基因表达更高。真皮成纤维细胞的衰老会减少成纤维细胞分泌的生长因子和细胞因子,这可能导致黑素细胞死亡和白癜风进展。然而,需要对更多患者进行进一步研究以证实成纤维细胞在白癜风发病机制中的作用。