Signalling pathways involved in ribonuclease-7 expression

Mohammed, Imran; Yeung, Aaron; Abedin, Asiya; Hopkinson, Andrew; Dua, Harminder S.

Abstract

Antimicrobial peptides are host defence molecules that play a potential role in preventing infection at the epithelial surfaces. Ribonuclease (RNase)-7 has been shown to possess a broad spectrum of microbicidal activity against various pathogens. Here, we demonstrate that RNase-7 protein is localised to the superficial layers of ocular surface cells and increased in response to interleukin (IL)-1β, suggesting an active role during inflammation related to ocular surface infection. Signal transduction pathways involved in RNase-7 expression are unknown. Involvement of transforming growth factor β-activated kinase-1 (TAK-1) activated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathway molecules [c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38] were studied because of their importance in infection and inflammation. Blocking the MAPKs resulted in inhibition of RNase-7 expression in response to IL-1β. However, RNase-7 induction by IL-1β was not affected by inhibiting the NF-κB signalling pathway. In conclusion, our results indicate that RNase-7 expression is specifically mediated via MAPKs but not NF-κB signalling pathways.

Citation

Mohammed, I., Yeung, A., Abedin, A., Hopkinson, A., & Dua, H. S. (2011). Signalling pathways involved in ribonuclease-7 expression. Cellular and Molecular Life Sciences, 68(11), 1941-1952. https://doi.org/10.1007/s00018-010-0540-2

• Journal Article Type: Article
• Acceptance Date: Sep 27, 2010
• Online Publication Date: Oct 22, 2010
• Publication Date: 2011-06
• Deposit Date: Jul 21, 2020
• Journal: Cellular and Molecular Life Sciences
• Print ISSN: 1420-682X
• Electronic ISSN: 1420-9071
• Publisher: Springer Verlag
• Peer Reviewed: Peer Reviewed
• Volume: 68
• Issue: 11
• Pages: 1941-1952
• DOI: https://doi.org/10.1007/s00018-010-0540-2
• Keywords: Molecular Medicine; Cell Biology; Molecular Biology; Pharmacology; Cellular and Molecular Neuroscience
• Public URL: https://nottingham-repository.worktribe.com/output/4781051
• Publisher URL: https://link.springer.com/article/10.1007/s00018-010-0540-2