The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Identification of MyD88 as a novel target of miR‐155, involved in negative regulation of Helicobacter pylori‐induced inflammation
Abstract
MicroRNA‐155 (miR‐155) has been implicated as a central regulator of the immune system. We have previously reported that miR‐155 negatively regulates Helicobacter pylori (H. pylori)‐induced inflammation, but the molecular mechanism of miR‐155 regulating the inflammation is not fully clear. Here, we identified myeloid differentiation protein 88 (MyD88) as a target gene of miR‐155, and found that miR‐155 decreased MyD88 expression at the protein but not the mRNA message level, suggesting that the miR‐155‐mediated inhibition is a post‐transcriptional event. Furthermore, the overexpression of miR‐155 led to significantly reduced IL‐8 production induced by H. pylori infection. Thus, we have demonstrated that miR‐155 can negatively regulate inflammation by targeting a key adaptor molecule MyD88 in inflammatory pathways.
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In the citing paper
“The miR-155 is a multifunctional microRNA and it can modulate inflammatory responses in both a positive and negative way [40-48].”
From miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses (2014) · cites this paper as [47]
In the citing paper
“Besides its positive role in NF-κB activation and subsequent pro-inflammatory response, accumulating evidence has demonstrated that it can constitute a negative feedback loop in the NF-κB signaling pathway by targeting multiple key proteins, which ultimately leads to repression of, or at least the limitation of NF-κB activation in response to viral or microbial stimuli [41,42,45-48].”
From miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses (2014) · cites this paper as [47]
Citations
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Cited by
Sorted by citations
MicroRNA-155 Promotes Autophagy to Eliminate Intracellular Mycobacteria by Targeting Rheb
Wang, J., Yang, K., Zhou, L., MinhaoWu, Wu, Y., Zhu, M., Lai, X., Chen, T., Feng, L., Li, M., et al. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003697 · Cited by 265
MicroRNAs: New Regulators of Toll-Like Receptor Signalling Pathways
He, X., Jing, Z., & Cheng, G. (2014) · BioMed Research International · doi:10.1155/2014/945169 · Cited by 238
Lai, L., Song, Y., Liu, Y., Chen, Q., Han, Q., Chen, W., Pan, T., Zhang, Y., Cao, X., & Wang, Q. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.445429 · Cited by 126
Pareek, S., Roy, S., Kumari, B., Jain, P., Banerjee, A., & Vrati, S. (2014) · Journal of Neuroinflammation · doi:10.1186/1742-2094-11-97 · Cited by 121
Metadata
- Authors
- Tang, B., Xiao, B., Liu, Z., Li, N., Zhu, E.-D., Li, B.-S., Xie, Q.-H., Zhuang, Y., Zou, Q.-M., & Mao, X.-H.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2010-02-26
- Volume
- 584
- Issue
- 8
- Pages
- 1481-1486
- ISSN
- 0014-5793
- 1873-3468
- Cited by
- 185
- References
- 2
- Language
- en
- Funders
- Chinese National Natural Science Foundation project (30770113)
- National Basic Research Program of China (973 Program) (2009CB522606)
- National High Technology Research and Development Program of China (863 Program) (2006AA02A208)
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