The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Induction of microRNA‐155 during Helicobacter pylori Infection and Its Negative Regulatory Role in the Inflammatory Response
Abstract
BACKGROUND: MicroRNAs (miRNAs) are small, noncoding RNAs that regulate gene expression at posttranscriptional level. H. pylori is a major human pathogenic bacterium in gastric mucosa. To date, the role of miRNAs in response to H. pylori infection has not been explored. METHODS: The expression profile of cellular miRNAs during H. pylori infection was analyzed by using microarray and quantitative reverse-transcriptase polymerase chain reaction. The potential target of miR-155 was identified by luciferase assay and Western blot. Promoter analysis and inhibitor experiment were used to investigate the pathway involved in the induction of miR-155. Examination of miR-155 function was performed by overexpression and inhibition of miR-155. RESULTS: H. pylori was able to increase the miR-155 expression in gastric epithelial cell lines and gastric mucosal tissues, and nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) pathway were required for the induction of miR-155. miR-155 may down-regulate IkappaB kinase epsilon, Sma- and Mad-related protein 2 (SMAD2), and Fas-associated death domain protein. Furthermore, the overexpression of miR-155 negatively regulated the release of interleukin-8 and growth-related oncogene-alpha. CONCLUSIONS: This study provides the first description of increased expression of miR-155 in H. pylori infection, and miR-155 may function as novel negative regulator that help to fine-tune the inflammation response of H. pylori infection.
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In the citing paper
“Similar observations were made by Xiao et al.[42] who reported a 3-fold induction of miR-155 and pro-inflammatory cytokine responses during Helicobacter pylori infection, whereas the overexpression of miR-155 negatively regulated the pro-inflammatory responses.”
From miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses (2014) · cites this paper as [42]
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 [42]
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 [42]
Citations
Cites
The functions of animal microRNAs
Ambros, V. (2004) · Nature · doi:10.1038/nature02871 · Cited by 10,728
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Requirement of bic/microRNA-155 for Normal Immune Function
Rodriguez, A., Vigorito, E., Clare, S., Warren, M. V., Couttet, P., Soond, D. R., van Dongen, S., Grocock, R. J., Das, P. P., Miska, E. A., et al. (2007) · Science · doi:10.1126/science.1139253 · Cited by 1,833
MicroRNAs and immunity: Novel players in the regulation of normal immune function and inflammation
Sonkoly, E., Ståhle, M., & Pivarcsi, A. (2008) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2008.01.005 · Cited by 523 · cited 1×
“There has been recent evidence regarding novel role of miRNAs in the regulation of immune system, including the development and differentiation of immune cells, antibody production, and innate immunity regulation [4, 5].”
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Rajaram, M. V. S., Ni, B., Morris, J. D., Brooks, M. N., Carlson, T. K., Bakthavachalu, B., Schoenberg, D. R., Torrelles, J. B., & Schlesinger, L. S. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1112660108 · Cited by 269
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
Self-citationMicroRNA-155 Is Required for Mycobacterium bovis BCG-Mediated Apoptosis of Macrophages
Ghorpade, D. S., Leyland, R., Kurowska-Stolarska, M., Patil, S. A., & Balaji, K. N. (2012) · Molecular and Cellular Biology · doi:10.1128/mcb.06597-11 · Cited by 142
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
Expression and functional importance of innate immune receptors by intestinal epithelial cells
Marques, R., & Boneca, I. G. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-011-0829-9 · Cited by 76
Noncoding RNAs regulate NF-κB signaling to modulate blood vessel inflammation
Cheng, H. S., Njock, M.-S., Khyzha, N., Dang, L. T., & Fish, J. E. (2014) · Frontiers in Genetics · doi:10.3389/fgene.2014.00422 · Cited by 69
Tay, H. L., Kaiko, G. E., Plank, M., Li, J., Maltby, S., Essilfie, A.-T., Jarnicki, A., Yang, M., Mattes, J., Hansbro, P. M., et al. (2015) · PLOS Pathogens · doi:10.1371/journal.ppat.1004549 · Cited by 67
Pandey, M., Ojha, D., Bansal, S., Rode, A. B., & Chawla, G. (2021) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2021.101003 · Cited by 23
Metadata
- Authors
- Xiao, B., Liu, Z., Li, B., Tang, B., Li, W., Guo, G., Shi, Y., Wang, F., Wu, Y., Tong, W., Guo, H., Mao, X., & Zou, Q.
- Venue
- The Journal of Infectious Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-09-15
- Volume
- 200
- Issue
- 6
- Pages
- 916-925
- ISSN
- 0022-1899
- 1537-6613
- Cited by
- 240
- References
- 5
- Language
- en
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