MiR-1294 suppresses ROS-dependent inflammatory response in atopic dermatitis via restraining STAT3/NF-κB pathway

• Published in: Cellular immunology 2022-01, Vol.371, p.104452-104452, Article 104452
• Main Authors: Yan, Chen, Ying, Jiang, lu, Wang, Changzhi, Yang, Qihong, Qian, Jingzhu, Mao, Dongjie, Sun, Tingting, Zhu
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis - immunology; Atopic dermatitis (AD); Cell Cycle - physiology; Cell Line; Cell Survival - physiology; Dermatitis, Atopic - genetics; Dermatitis, Atopic - immunology; Dermatitis, Atopic - pathology; Enzyme-Linked Immunosorbent Assay; Female; HaCaT Cells; Humans; Inflammation - immunology; Inflammatory response; Interferon-gamma - metabolism; Mice; MicroRNAs - genetics; MiR-1294; NF-kappa B - metabolism; NF-κB pathway; Reactive Oxygen Species - metabolism; Skin - immunology; Skin - pathology; STAT3; STAT3 Transcription Factor - genetics; STAT3 Transcription Factor - metabolism; Tight Junctions - physiology; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1016/j.cellimm.2021.104452

•miR-1294 acts as a key role in regulation of inflammatory response atopic dermatitis.•miR-1294 attenuates ROS-dependent inflammatory response by inhibiting STAT3/NF-κB pathway. Atopic dermatitis (AD) is a common inflammatory skin disorder that affects children and adults. Despite the pathology of AD involves in immune dysfunction and epidermal barrier function destruction has been found, the mechanism of immune activation and barrier damage remain largely unknown. In the present study, The TNF-α/IFN-γ-stimulated HaCaTs, organotypic AD-like 3D skin equivalents and AD-like mouse model were constructed. The mRNA, histological morphology, protein levels, cytokines were detected by real-time quantitative polymerasechain reaction (RT-qPCR), hematoxylin and eosin (H & E) staining, Immunohistochemistry (IHC), immunoblotting, immunofluorescence (IF) staining, and enzyme linked immunosorbent assay (ELISA), respectively. Cell viability, cell cycle, and apoptosis were respectively calculated using a Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and flow cytometry. A dual-luciferase reporter gene system was used to investigate the relationship between miR-1294 and STAT3. Compared with the control group, the expression of miR-1294 decreased in TNF-α/IFN-γ-stimulated HaCaTs (P