Investigation of the pathogenesis of ADAR1 gene in dyschromatosis symmetrica hereditaria

descriptionPublicationkeyboard_double_arrow_right Article 01 Feb 2024 English Publisher:WileyJournal:Experimental Dermatology, volume 33 (issn: 0906-6705, eissn: 1600-0625,

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Authors: Jia Zhang; Chengyi Jiang; Zhen Wang; Biqing Fang; Jin He; Ming Li;

doi: 10.1111/exd.15031

pmid: 38375898

Investigation of the pathogenesis of ADAR1 gene in dyschromatosis symmetrica hereditaria

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Abstract

AbstractThe pathogenesis of dyschromatosis symmetrica hereditaria (DSH) has not been well defined. In this study, we sought to investigate the influence of the ADAR1 gene on DSH both in vitro and in vivo. Morpholino knockdown of adar1 in zebrafish produced phenotypes characterized by polarity changes, and abnormal migration and distribution of melanocytes. Differential expression of C‐KIT and distinct patterns of apoptosis between hyperpigmented and hypopigmented areas in DSH patient were detected by means of immunohistochemical methods and TUNEL assays, respectively. This study revealed that adar1 knockdown in a zebrafish model resulted in abnormal migration and changes in the cell polarity of melanocytes, and provided novel insight into the mechanism of DSH pathogenesis.

Related Organizations

Shanghai Jiao Tong University
China (People's Republic of)
XinHua Hospital
China (People's Republic of)

Keywords

Adenosine Deaminase, Mutation, Animals, Humans, RNA-Binding Proteins, Zebrafish Proteins, Pigmentation Disorders, Zebrafish, Pedigree

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