The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
microRNA miR-144 modulates oxidative stress tolerance and associates with anemia severity in sickle cell disease
Open accessAbstract
Although individuals with homozygous sickle cell disease (HbSS) share the same genetic mutation, the severity and manifestations of this disease are extremely heterogeneous. We have previously shown that the microRNA expression in normal and HbSS erythrocytes exhibit dramatic differences. In this study, we identify a subset of HbSS patients with higher erythrocytic miR-144 expression and more severe anemia. HbSS erythrocytes are known to have reduced tolerance for oxidative stress, yet the basis for this phenotype remains unknown. This study reveals that miR-144 directly regulates nuclear factor-erythroid 2-related factor 2, a central regulator of cellular response to oxidative stress, and modulates the oxidative stress response in K562 cell line and primary erythroid progenitor cells. We further demonstrate that increased miR-144 is associated with reduced NRF2 levels in HbSS reticulocytes and with decreased glutathione regeneration and attenuated antioxidant capacity in HbSS erythrocytes, thereby providing a possible mechanism for the reduced oxidative stress tolerance and increased anemia severity seen in HbSS patients. Taken together, our findings suggest that erythroid microRNAs can serve as genetic modifiers of HbS-related anemia and can provide novel insights into the clinical heterogeneity and pathobiology of sickle cell disease.
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Itoh, K., Chiba, T., Takahashi, S., Ishii, T., Igarashi, K., Katoh, Y., Oyake, T., Hayashi, N., Satoh, K., Hatayama, I., et al. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1997.6943 · Cited by 3,999
Cell Survival Responses to Environmental Stresses Via the Keap1-Nrf2-ARE Pathway
Kensler, T. W., Wakabayashi, N., & Biswal, S. (2007) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.46.120604.141046 · Cited by 3,630
Mortality in sickle cell disease. Life expectancy and risk factors for early death
Platt, O. S., Brambilla, D. J., Rosse, W. F., Milner, P. F., Castro, O., Steinberg, M. H., & Klug, P. P. (1994) · New England Journal of Medicine · doi:10.1056/nejm199406093302303 · Cited by 3,320
Nrf2–Keap1 defines a physiologically important stress response mechanism
Motohashi, H., & Yamamoto, M. (2004) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2004.09.003 · Cited by 1,725
Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression
Neumann, C. A., Krause, D. S., Carman, C. V., Das, S., Dubey, D. P., Abraham, J. L., Bronson, R. T., Fujiwara, Y., Orkin, S. H., & Van Etten, R. A. (2003) · Nature · doi:10.1038/nature01819 · Cited by 801
Acute Chest Syndrome in Sickle Cell Disease: Clinical Presentation and Course
Vichinsky, E. P., Styles, L. A., Colangelo, L. H., Wright, E. C., Castro, O., Nickerson, B., & Disease, T. C. S. O. S. C. (1997) · Blood · doi:10.1182/blood.v89.5.1787 · Cited by 573
Targeted disruption of Nrf2 causes regenerative immune-mediated hemolytic anemia
Lee, J.-M., Chan, K., Kan, Y. W., & Johnson, J. A. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0403620101 · Cited by 120
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Loboda, A., Damulewicz, M., Pyza, E., Jozkowicz, A., & Dulak, J. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2223-0 · Cited by 2,632
NRF2, a Transcription Factor for Stress Response and Beyond
He, F., Ru, X., & Wen, T. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21134777 · Cited by 1,820
Nrf2 signaling pathway: pivotal roles in inflammation
Ahmed, S. M. U., Luo, L., Namani, A., Wang, X. J., & Tang, X. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.005 · Cited by 1,794
The emerging role of the Nrf2–Keap1 signaling pathway in cancer
Jaramillo, M. C., & Zhang, D. D. (2013) · Genes & Development · doi:10.1101/gad.225680.113 · Cited by 1,297
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Metadata
- Authors
- Sangokoya, C., Telen, M. J., & Chi, J.-T.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2010-11-18
- Volume
- 116
- Issue
- 20
- Pages
- 4338-4348
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2005645711
- Cited by
- 357
- References
- 7
- FWCI
- 8.68
- Type
- journal article
- Language
- en
- Open access
- green
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- Sangokoya, C., Telen, M. J., & Chi, J.-T. (2010). microRNA miR-144 modulates oxidative stress tolerance and associates with anemia severity in sickle cell disease. Blood. https://doi.org/10.1182/blood-2009-04-214817
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