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The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis

Open access
Kurowska-Stolarska, Mariola, Alivernini, Stefano, Ballantine, Lucy E., Asquith, Darren L., Millar, Neal L., Gilchrist, Derek S., Reilly, James, Ierna, Michelle, Fraser, Alasdair R., Stolarski, Bartosz, McSharry, Charles, Hueber, Axel J., Baxter, Derek, Hunter, John, Gay, Steffen, Liew, Foo Y., McInnes, Iain B.·2011·Proceedings of the National Academy of Sciences

Abstract

MicroRNA (miRNA) species (miR) regulate mRNA translation and are implicated as mediators of disease pathology via coordinated regulation of molecular effector pathways. Unraveling miR disease-related activities will facilitate future therapeutic interventions. miR-155 recently has been identified with critical immune regulatory functions. Although detected in articular tissues, the functional role of miR-155 in inflammatory arthritis has not been defined. We report here that miR-155 is up-regulated in synovial membrane and synovial fluid (SF) macrophages from patients with rheumatoid arthritis (RA). The increased expression of miR-155 in SF CD14 + cells was associated with lower expression of the miR-155 target, Src homology 2-containing inositol phosphatase-1 (SHIP-1), an inhibitor of inflammation. Similarly, SHIP-1 expression was decreased in CD68 + cells in the synovial lining layer in RA patients as compared with osteoarthritis patients. Overexpression of miR-155 in PB CD14 + cells led to down-regulation of SHIP-1 and an increase in the production of proinflammatory cytokines. Conversely, inhibition of miR-155 in RA synovial CD14 + cells reduced TNF-α production. Finally, miR-155–deficient mice are resistant to collagen-induced arthritis, with profound suppression of antigen-specific Th17 cell and autoantibody responses and markedly reduced articular inflammation. Our data therefore identify a role of miR-155 in clinical and experimental arthritis and suggest that miR-155 may be an intriguing therapeutic target.

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Show all 9 references

Research works printed but not linked: 28

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Metadata

Authors
Kurowska-Stolarska, M., Alivernini, S., Ballantine, L. E., Asquith, D. L., Millar, N. L., Gilchrist, D. S., Reilly, J., Ierna, M., Fraser, A. R., Stolarski, B., McSharry, C., Hueber, A. J., Baxter, D., Hunter, J., Gay, S., Liew, F. Y., & McInnes, I. B.
Venue
Proceedings of the National Academy of Sciences
Published
2011-06-20
Volume
108
Issue
27
Pages
11193-11198
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2059695215
Cited by
641
References
9
FWCI
41.64
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis. https://app.cochat.ai/papers/10.1073/pnas.1019536108
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Kurowska-Stolarska, M., Alivernini, S., Ballantine, L. E., Asquith, D. L., Millar, N. L., Gilchrist, D. S., Reilly, J., Ierna, M., Fraser, A. R., Stolarski, B., McSharry, C., Hueber, A. J., Baxter, D., Hunter, J., Gay, S., Liew, F. Y., & McInnes, I. B. (2011). MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1019536108

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.