Inhibition of miR-92d-3p enhances inflammation responses in genetically improved farmed tilapia (GIFT, Oreochromis niloticus) with Streptococcus iniae infection by modulating complement C3

• Published in: Fish & shellfish immunology 2017-04, Vol.63, p.367-375
• Main Authors: Qiang, Jun, Tao, Yi-Fan, He, Jie, Li, Hong-Xia, Xu, Pao, Bao, Jin-Wen, Sun, Yi-Lan
• Format: Article
• Language: English
• Subjects: Animals; Cichlids - genetics; Complement C3; Complement C3 - genetics; Complement C3 - metabolism; Fish Diseases - genetics; Fish Diseases - immunology; Fish Diseases - microbiology; Fish Proteins - genetics; Fish Proteins - metabolism; Gene Expression Regulation; GIFT; Head kidney; Immunity, Innate; Inflammation - genetics; Inflammation - immunology; Inflammation - microbiology; Inflammation - veterinary; Inflammatory response; MicroRNAs - genetics; MicroRNAs - metabolism; miR-92d-3p; Streptococcal Infections - genetics; Streptococcal Infections - immunology; Streptococcal Infections - microbiology; Streptococcal Infections - veterinary; Streptococcus iniae - physiology
• ISSN: 1050-4648; 1095-9947
• DOI: 10.1016/j.fsi.2017.02.036

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate target gene expression by binding to the 3′-untranslated regions (3′-UTRs) of their target mRNAs. The miR-92 family is an important miRNA family, which was discovered to be related to regulation of tumor proliferation, apoptosis, invasion, and metastasis. Inhibition of miR-92d-3p was found previously in head kidney of genetically improved farmed tilapia (GIFT, Oreochromis niloticus) exposed to Streptococcus iniae infection. In this study, we found that miR-92d-3p regulated complement C3 mRNA levels by binding to its 3′-UTR by 3′-UTR luciferase reporter assay, and reduced miR-92d-3p expression resulted in increased C3 mRNA levels. We detected a negative relationship between the expression levels of miR-92d-3p and C3 in GIFT injected with miRNA antagomir. We performed in vivo functional analysis by miR-92d-3p silencing. Inhibition of miR-92d-3p levels in GIFT head kidney caused a significant increase in C3 expression, which consequently increased the white blood cell counts and interleukin-1β, tumor necrosis factor-α, and interferon-γ mRNA levels, all of which may help to activate the inflammatory response in GIFT post-infection with S. iniae. Our findings indicate that miR-92d-3p regulated C3 levels by binding with the C3 mRNA 3′-UTR, and this interaction affected S. iniae infection induction and the immune response in GIFT. We concluded that miR-92d-3p plays an important role in modulating the inflammatory response in GIFT head kidney. Our findings may contribute to understanding the mechanisms of miRNA-mediated gene regulation in tilapia in response to S. iniae infection. •miR-92d-3p regulated GIFT C3 by directly targeting C3 3′UTR.•miR-92d-3p level was conversely related to C3 level under S. iniae infection.•miR-92d-3p silencing up-regulated C3 mRNA expression.•miR-92d-3p loss activated inflammatory response and WBC counts.