Abstract
Background Vitiligo is a relatively common pigmentation disorder in which the skin melanocytes are lost or destroyed. Experimental downregulation of long noncoding RNA H19 (lnc RNA H19) in keratinocytes promoted melanocytes melanogenesis. lnc RNA H19 acts as an important regulator for micro-RNA let7a (miRNA let7a). miRNA let7a has a powerful role in regulation of cell survival and inducing cell apoptosis.Objectives This study was performed to clarify the suggested role of lnc RNA H19 and miRNA let7a derived from human skin exosomes in vitiligo pathogenesis.Patients and methods The study included 50 patients with vitiligo vulgaris and 50 healthy volunteers serving as controls. From all patients, 4-mm punch skin biopsies were taken. Skin biopsies were examined for lnc RNA H19 and miRNA let7a genes expression using RT-PCR technique.Results The expression of lnc RNA H19 and miRNA let7a in vitiligo lesions (1.736±0.84 and 6.7±2.26 pg/mg, respectively) was significantly higher than their expression in controls (0.8462±0.3483 and 1.514± 0.9202 pg/mg, respectively) (P<0.001). A significant positive correlation was found between the expression of lnc RNA H19 and the disease activity (P=0.0382). Additionally, a positive correlation was detected between the expression of miRNA let7a and the disease duration (P<0.0306).Conclusions We can conclude that upregulation of lnc RNA H19 and miRNA let7a gene expression describes their possible role in the pathogenesis of vitiligo.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Journal of the Egyptian Women's Dermatologic Society
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.